But because people with diabetes do get heart attacks at a rate higher than the general population, it would be nice to know what markers could be trusted to help you know your real risk.
Your A1c and, even more strongly, your post-meal blood sugar levels are helpful in assessing risk. But some people with well controlled blood sugars do develop heart disease. So some recent research published in the journal Diabetes might point to another safe tool you can use to assess your own, personal risk.
You can read the abstract of the study here:
Apolipoprotein B but not LDL Cholesterol Is Associated With Coronary Artery Calcification in Type 2 Diabetic Whites Seth S. Martin et al. Diabetes. Diabetes August 2009 vol. 58 no. 8 1887-1892 doi: 10.2337/db08-1794
Apolipoproteins are proteins that are produced in the intestines and liver. They attach to cholesterol particles released by digestion and are what allow these particles to be transported through the body. Because apolipoproteuns fit receptors on various cells, they play a large part in the processes that allow cholesterol to be metabolized.
Apolipoprotein B (APO B) is the lipoprotein that attaches to LDL cholesterol and helps transport it around the body. It has long been known that it provides a better measure of cardiac risk than does the measurement of LDL cholesterol. This is not news. You can read about that in a study published in 2002:
How, when, and why to use apolipoprotein B in clinical practice. Sniderman Allan D. The American journal of cardiology, ISSN 0002-9149 2002, vol. 90, no 8A (86 p.) (32 ref.), pp. 48i-54i
The reason APO B is useful is so useful is that there is one molecule of APO B associated with every particle of LDL cholesterol. This means that the measurement of APO B points the the actual number of LDL particles. This is especially important because The usual LDL measure you get on your lab report does not. In fact, the LDL value on your cholesterol test result isn't an actual measure of your LDL. It is a calculated number that is derived by applying a simplistic formula to the triglycerides and total Cholesterol that were measured. Because it is a calculation, not a measurement, it can give either erroneously low or erroneously high readings depending on the size of your LDL particles.
Dangerous LDL comes in small particles which are prone to attach to arteries. Very large fluffy LDL molecule tends not to bond to your arteries. The LDL calculation apparently gives something like the total volume of your LDL, so if, like me, you have a modest number of very large fluffy molecules the formula gives an extremely high LDL figure while someone with a lot of very small dense LDL may be told they have a low, misleadingly comforting LDL number.
This is one reason why fully one half of people who have heart attacks have "normal" cholesterol--because just measuring the amount of cholesterol is worthless. You have to know how many cholesterol particles you have to better understand risk since small dense LDL does correlate with your risk of having cholesterol clog your arteries.
So while it isn't new that your APO B value is a useful indicator of risk, the new Diabetes study is useful because it finds that APO B is the only LDL test result that provides useful information to people with Type 2 diabetes.
This may be because most people with diabetes have extremely high triglicerides which skew the LDL calculation. If you have normalized your blood sugar this may mean that the APO B test is not quite as useful for you.
The other reason that the APO B test might be more useful for people with diabetes is that they are usually put on statins which can cut down on the amount of LDL they secrete without changing the characteristics of those LDL particles. So while LDL may drop after taking a statin, the person may still be making a lot of very tiny, dense LDL molecules that give them a heightened risk of clogged arteries, even though their LDL numbers went down.
Reading this study, you might ask yourself, "Why not just get a CAC scan, as Dr. Davis of the Heart Scan Blog (no longer online) suggests. The answer is that the CAC is expensive and may not be covered by insurance. In addition, depending on who offers it, it may expose you to significant amounts of radiation. Dr. Davis points out this doesn't have to be the case, but in practice you may not have the expertise to know if the CAC scanning available to you is being done with low radiation equipment or not, and sadly, you can't trust the people doing the test to give you a trustworthy answer because they have a strong financial interest in selling you the scan.
So if you have a high risk of heart attack and are trying to decide if a heart scan would be worth the money and the radiation exposure, you might consider asking your doctor to do the APO B test to help you get a better feel for whether the scan would provide useful information. If the APO B number is high, it is more likely you would see evidence of significant calcification in your arteries. If you need to see the picture to get motivated to do something about this issue, the scan might be worthwhile.
But this raises an important issue. Medical testing is a waste of money unless result A will lead to your adopting a different treatment than result B. It should never be done just to satisfy your curiosity.
If you believe you have a higher risk of heart attack than a normal person you may already be doing all the things people can do: cutting way down on carbs, monitoring your blood sugar and aiming for the lowest possible A1c, keeping your blood pressure normal, supplementing with Vitamin D, and exercising. If you have had your C-reactive protein measured and it was high, you may already be on a statin.
So before you invest in further cardiac testing you have to ask yourself, "What will I do if the test comes back with a value suggesting I am developing heart disease?"
The answer may be, become obsessive and depressed about health in a way that does not improve the quality of your life and this is the last thing that you want. You can live every day of the next 30 years waiting for your heart attack, or you can do what you can do and extract the maximum pleasure out of today and the days that follow it. My dad lived for 30 years after a diagnosis of "severe heart disease." He did end up having a heart attack--28 years after his diagnosis, at the age of 98. He died of a fall two years later. He led an active life for those last 30 years and would have been far better off without the diagnosis since he spent 28 years waiting for that heart attack--and threatening to have it any time anyone in the family disagreed with him!
Heart disease is a valid concern for people with diabetes, but I hear from far too many recently diagnosed people who are terrified that their diabetes diagnosis is a death sentence. It isn't-if you keep your blood sugar under control.
As I have mentioned in an earlier blog post, researchers are seeing far fewer heart attacks than expected in large scale studies. Many reports about cardiovascular disease use the "risk" statistic, which produces a big, scary number rather than the incidence per 1000 people number which gives a much smaller, more reasonable number.
So if you are already taking the steps a prudent person would take, there probably is no point in pursuing ever more diagnostic tests. If the tests could make a difference in your treatment plan--for example, convince you to take an expensive, side-effect rich statin--they might be worth consideration.
To summarize data I have discussed on the main Blood Sugar 101 web sit, here are the test results most indicative of cardiovascular health:
1. Triglyceride levels. Under 150 is the minimum, much lower is much better. Triglycerides should come down as you cut your carbohydrate levels because triglycerides are the product of the digestion of carbohydrate. If they don't come down with low carb dieting and tight blood sugar control, you should have your doctor explore why.
2. Blood pressure. Keep it under 140/85 and demand aggressive therapy from your doctor if it stays higher for any period of time.
3. Cardiac Specific C-Reactive Protein. High levels point to inflammation in your arteries and suggest you might be one of the people who would benefit from taking a statin.
4. Apo B which can help you interpret your LDL score.
5. LDL particle size is a helpful test since LDL particle size appears to be a very good indicator of whether your LDL will caused clogged arteries but very few doctors will perform it or have even heard about it.
6. EKG to determine if you have had a silent heart attack in the past.
July 31, 2009
Apolipoprotein- B But not LDL Cholesterol Linked to Artery Calcium Build Up
Many of my readers know that despite their doctors' obsession with their Cholesterol levels the evidence has never supported the idea that cholesterol levels predict heart attack. You can read about this issue, with resarch citations, on this page: A1c And Post-Meal Blood Sugar Predict Heart Attack or if you are looking for total immersion in the research regarding cholesterol and cardiovascular disease you can get it from reading Gary Taubes' monumental book, Good Calories, Bad Calories.
But because people with diabetes do get heart attacks at a rate higher than the general population, it would be nice to know what markers could be trusted to help you know your real risk.
Your A1c and, even more strongly, your post-meal blood sugar levels are helpful in assessing risk. But some people with well controlled blood sugars do develop heart disease. So some recent research published in the journal Diabetes might point to another safe tool you can use to assess your own, personal risk.
You can read the abstract of the study here:
Apolipoprotein B but not LDL Cholesterol Is Associated With Coronary Artery Calcification in Type 2 Diabetic Whites Seth S. Martin et al. Diabetes. Diabetes August 2009 vol. 58 no. 8 1887-1892 doi: 10.2337/db08-1794
Apolipoproteins are proteins that are produced in the intestines and liver. They attach to cholesterol particles released by digestion and are what allow these particles to be transported through the body. Because apolipoproteuns fit receptors on various cells, they play a large part in the processes that allow cholesterol to be metabolized.
Apolipoprotein B (APO B) is the lipoprotein that attaches to LDL cholesterol and helps transport it around the body. It has long been known that it provides a better measure of cardiac risk than does the measurement of LDL cholesterol. This is not news. You can read about that in a study published in 2002:
How, when, and why to use apolipoprotein B in clinical practice. Sniderman Allan D. The American journal of cardiology, ISSN 0002-9149 2002, vol. 90, no 8A (86 p.) (32 ref.), pp. 48i-54i
The reason APO B is useful is so useful is that there is one molecule of APO B associated with every particle of LDL cholesterol. This means that the measurement of APO B points the the actual number of LDL particles. This is especially important because The usual LDL measure you get on your lab report does not. In fact, the LDL value on your cholesterol test result isn't an actual measure of your LDL. It is a calculated number that is derived by applying a simplistic formula to the triglycerides and total Cholesterol that were measured. Because it is a calculation, not a measurement, it can give either erroneously low or erroneously high readings depending on the size of your LDL particles.
Dangerous LDL comes in small particles which are prone to attach to arteries. Very large fluffy LDL molecule tends not to bond to your arteries. The LDL calculation apparently gives something like the total volume of your LDL, so if, like me, you have a modest number of very large fluffy molecules the formula gives an extremely high LDL figure while someone with a lot of very small dense LDL may be told they have a low, misleadingly comforting LDL number.
This is one reason why fully one half of people who have heart attacks have "normal" cholesterol--because just measuring the amount of cholesterol is worthless. You have to know how many cholesterol particles you have to better understand risk since small dense LDL does correlate with your risk of having cholesterol clog your arteries.
So while it isn't new that your APO B value is a useful indicator of risk, the new Diabetes study is useful because it finds that APO B is the only LDL test result that provides useful information to people with Type 2 diabetes.
This may be because most people with diabetes have extremely high triglicerides which skew the LDL calculation. If you have normalized your blood sugar this may mean that the APO B test is not quite as useful for you.
The other reason that the APO B test might be more useful for people with diabetes is that they are usually put on statins which can cut down on the amount of LDL they secrete without changing the characteristics of those LDL particles. So while LDL may drop after taking a statin, the person may still be making a lot of very tiny, dense LDL molecules that give them a heightened risk of clogged arteries, even though their LDL numbers went down.
Reading this study, you might ask yourself, "Why not just get a CAC scan, as Dr. Davis of the Heart Scan Blog (no longer online) suggests. The answer is that the CAC is expensive and may not be covered by insurance. In addition, depending on who offers it, it may expose you to significant amounts of radiation. Dr. Davis points out this doesn't have to be the case, but in practice you may not have the expertise to know if the CAC scanning available to you is being done with low radiation equipment or not, and sadly, you can't trust the people doing the test to give you a trustworthy answer because they have a strong financial interest in selling you the scan.
So if you have a high risk of heart attack and are trying to decide if a heart scan would be worth the money and the radiation exposure, you might consider asking your doctor to do the APO B test to help you get a better feel for whether the scan would provide useful information. If the APO B number is high, it is more likely you would see evidence of significant calcification in your arteries. If you need to see the picture to get motivated to do something about this issue, the scan might be worthwhile.
But this raises an important issue. Medical testing is a waste of money unless result A will lead to your adopting a different treatment than result B. It should never be done just to satisfy your curiosity.
If you believe you have a higher risk of heart attack than a normal person you may already be doing all the things people can do: cutting way down on carbs, monitoring your blood sugar and aiming for the lowest possible A1c, keeping your blood pressure normal, supplementing with Vitamin D, and exercising. If you have had your C-reactive protein measured and it was high, you may already be on a statin.
So before you invest in further cardiac testing you have to ask yourself, "What will I do if the test comes back with a value suggesting I am developing heart disease?"
The answer may be, become obsessive and depressed about health in a way that does not improve the quality of your life and this is the last thing that you want. You can live every day of the next 30 years waiting for your heart attack, or you can do what you can do and extract the maximum pleasure out of today and the days that follow it. My dad lived for 30 years after a diagnosis of "severe heart disease." He did end up having a heart attack--28 years after his diagnosis, at the age of 98. He died of a fall two years later. He led an active life for those last 30 years and would have been far better off without the diagnosis since he spent 28 years waiting for that heart attack--and threatening to have it any time anyone in the family disagreed with him!
Heart disease is a valid concern for people with diabetes, but I hear from far too many recently diagnosed people who are terrified that their diabetes diagnosis is a death sentence. It isn't-if you keep your blood sugar under control.
As I have mentioned in an earlier blog post, researchers are seeing far fewer heart attacks than expected in large scale studies. Many reports about cardiovascular disease use the "risk" statistic, which produces a big, scary number rather than the incidence per 1000 people number which gives a much smaller, more reasonable number.
So if you are already taking the steps a prudent person would take, there probably is no point in pursuing ever more diagnostic tests. If the tests could make a difference in your treatment plan--for example, convince you to take an expensive, side-effect rich statin--they might be worth consideration.
To summarize data I have discussed on the main Blood Sugar 101 web sit, here are the test results most indicative of cardiovascular health:
1. Triglyceride levels. Under 150 is the minimum, much lower is much better. Triglycerides should come down as you cut your carbohydrate levels because triglycerides are the product of the digestion of carbohydrate. If they don't come down with low carb dieting and tight blood sugar control, you should have your doctor explore why.
2. Blood pressure. Keep it under 140/85 and demand aggressive therapy from your doctor if it stays higher for any period of time.
3. Cardiac Specific C-Reactive Protein. High levels point to inflammation in your arteries and suggest you might be one of the people who would benefit from taking a statin.
4. Apo B which can help you interpret your LDL score.
5. LDL particle size is a helpful test since LDL particle size appears to be a very good indicator of whether your LDL will caused clogged arteries but very few doctors will perform it or have even heard about it.
6. EKG to determine if you have had a silent heart attack in the past.
But because people with diabetes do get heart attacks at a rate higher than the general population, it would be nice to know what markers could be trusted to help you know your real risk.
Your A1c and, even more strongly, your post-meal blood sugar levels are helpful in assessing risk. But some people with well controlled blood sugars do develop heart disease. So some recent research published in the journal Diabetes might point to another safe tool you can use to assess your own, personal risk.
You can read the abstract of the study here:
Apolipoprotein B but not LDL Cholesterol Is Associated With Coronary Artery Calcification in Type 2 Diabetic Whites Seth S. Martin et al. Diabetes. Diabetes August 2009 vol. 58 no. 8 1887-1892 doi: 10.2337/db08-1794
Apolipoproteins are proteins that are produced in the intestines and liver. They attach to cholesterol particles released by digestion and are what allow these particles to be transported through the body. Because apolipoproteuns fit receptors on various cells, they play a large part in the processes that allow cholesterol to be metabolized.
Apolipoprotein B (APO B) is the lipoprotein that attaches to LDL cholesterol and helps transport it around the body. It has long been known that it provides a better measure of cardiac risk than does the measurement of LDL cholesterol. This is not news. You can read about that in a study published in 2002:
How, when, and why to use apolipoprotein B in clinical practice. Sniderman Allan D. The American journal of cardiology, ISSN 0002-9149 2002, vol. 90, no 8A (86 p.) (32 ref.), pp. 48i-54i
The reason APO B is useful is so useful is that there is one molecule of APO B associated with every particle of LDL cholesterol. This means that the measurement of APO B points the the actual number of LDL particles. This is especially important because The usual LDL measure you get on your lab report does not. In fact, the LDL value on your cholesterol test result isn't an actual measure of your LDL. It is a calculated number that is derived by applying a simplistic formula to the triglycerides and total Cholesterol that were measured. Because it is a calculation, not a measurement, it can give either erroneously low or erroneously high readings depending on the size of your LDL particles.
Dangerous LDL comes in small particles which are prone to attach to arteries. Very large fluffy LDL molecule tends not to bond to your arteries. The LDL calculation apparently gives something like the total volume of your LDL, so if, like me, you have a modest number of very large fluffy molecules the formula gives an extremely high LDL figure while someone with a lot of very small dense LDL may be told they have a low, misleadingly comforting LDL number.
This is one reason why fully one half of people who have heart attacks have "normal" cholesterol--because just measuring the amount of cholesterol is worthless. You have to know how many cholesterol particles you have to better understand risk since small dense LDL does correlate with your risk of having cholesterol clog your arteries.
So while it isn't new that your APO B value is a useful indicator of risk, the new Diabetes study is useful because it finds that APO B is the only LDL test result that provides useful information to people with Type 2 diabetes.
This may be because most people with diabetes have extremely high triglicerides which skew the LDL calculation. If you have normalized your blood sugar this may mean that the APO B test is not quite as useful for you.
The other reason that the APO B test might be more useful for people with diabetes is that they are usually put on statins which can cut down on the amount of LDL they secrete without changing the characteristics of those LDL particles. So while LDL may drop after taking a statin, the person may still be making a lot of very tiny, dense LDL molecules that give them a heightened risk of clogged arteries, even though their LDL numbers went down.
Reading this study, you might ask yourself, "Why not just get a CAC scan, as Dr. Davis of the Heart Scan Blog (no longer online) suggests. The answer is that the CAC is expensive and may not be covered by insurance. In addition, depending on who offers it, it may expose you to significant amounts of radiation. Dr. Davis points out this doesn't have to be the case, but in practice you may not have the expertise to know if the CAC scanning available to you is being done with low radiation equipment or not, and sadly, you can't trust the people doing the test to give you a trustworthy answer because they have a strong financial interest in selling you the scan.
So if you have a high risk of heart attack and are trying to decide if a heart scan would be worth the money and the radiation exposure, you might consider asking your doctor to do the APO B test to help you get a better feel for whether the scan would provide useful information. If the APO B number is high, it is more likely you would see evidence of significant calcification in your arteries. If you need to see the picture to get motivated to do something about this issue, the scan might be worthwhile.
But this raises an important issue. Medical testing is a waste of money unless result A will lead to your adopting a different treatment than result B. It should never be done just to satisfy your curiosity.
If you believe you have a higher risk of heart attack than a normal person you may already be doing all the things people can do: cutting way down on carbs, monitoring your blood sugar and aiming for the lowest possible A1c, keeping your blood pressure normal, supplementing with Vitamin D, and exercising. If you have had your C-reactive protein measured and it was high, you may already be on a statin.
So before you invest in further cardiac testing you have to ask yourself, "What will I do if the test comes back with a value suggesting I am developing heart disease?"
The answer may be, become obsessive and depressed about health in a way that does not improve the quality of your life and this is the last thing that you want. You can live every day of the next 30 years waiting for your heart attack, or you can do what you can do and extract the maximum pleasure out of today and the days that follow it. My dad lived for 30 years after a diagnosis of "severe heart disease." He did end up having a heart attack--28 years after his diagnosis, at the age of 98. He died of a fall two years later. He led an active life for those last 30 years and would have been far better off without the diagnosis since he spent 28 years waiting for that heart attack--and threatening to have it any time anyone in the family disagreed with him!
Heart disease is a valid concern for people with diabetes, but I hear from far too many recently diagnosed people who are terrified that their diabetes diagnosis is a death sentence. It isn't-if you keep your blood sugar under control.
As I have mentioned in an earlier blog post, researchers are seeing far fewer heart attacks than expected in large scale studies. Many reports about cardiovascular disease use the "risk" statistic, which produces a big, scary number rather than the incidence per 1000 people number which gives a much smaller, more reasonable number.
So if you are already taking the steps a prudent person would take, there probably is no point in pursuing ever more diagnostic tests. If the tests could make a difference in your treatment plan--for example, convince you to take an expensive, side-effect rich statin--they might be worth consideration.
To summarize data I have discussed on the main Blood Sugar 101 web sit, here are the test results most indicative of cardiovascular health:
1. Triglyceride levels. Under 150 is the minimum, much lower is much better. Triglycerides should come down as you cut your carbohydrate levels because triglycerides are the product of the digestion of carbohydrate. If they don't come down with low carb dieting and tight blood sugar control, you should have your doctor explore why.
2. Blood pressure. Keep it under 140/85 and demand aggressive therapy from your doctor if it stays higher for any period of time.
3. Cardiac Specific C-Reactive Protein. High levels point to inflammation in your arteries and suggest you might be one of the people who would benefit from taking a statin.
4. Apo B which can help you interpret your LDL score.
5. LDL particle size is a helpful test since LDL particle size appears to be a very good indicator of whether your LDL will caused clogged arteries but very few doctors will perform it or have even heard about it.
6. EKG to determine if you have had a silent heart attack in the past.
July 29, 2009
Device Makers New Code of Ethics Forbids Gifts or Entertainment--for Medical Care Providers
Jim Purdy commented on the last post that just like medical care providers, we medical bloggers need to consider adopting a code of ethics. This sent me off on some research about existing codes of ethics involving corporate gifts, and what a surprise that turned up!
It turns out that the medical device manufacturing community's trade group, AdvaMed, proposed a Code of Ethics for its members in December 2008 which specifically banned all gifts or providing of entertainment to medical care providers.
AdvaMe is short for the Advanced Medical Technology Association, a trade group that claims its members "produce nearly 90 percent of the health care technology purchased annually in the United States and more than 50 percent purchased annually around the world."
Here's what's included in its new Code of Ethics:
Note that the code only applies to "health care providers." Not bloggers or those who maintain online support communities. Which might just have something to do with why a medical device maker is suddenly so interested in us humble bloggers.
Doctors are educated highly-paid professionals who, if anything, we would expect to be less influenced by small gifts and junkets, since they can well afford to spend their own money for such things. But it turns out small gifts have a subtle but very effective impact even on wealthy physicians.
You can read a good summary of research documenting how drug company gifts and junkets affect prescribing information in the following journal article. Follow the footnotes to find the studies summarized:
Do Drug Company Do drug company promotions influence physician behavior? Bob Goodman. West J Med.(BMJ) 2001 April; 174(4): 232–233.
How much more likely are we bloggers to be manipulated by drug and device companies?
Many of us earn very modest incomes or are retired. We make huge sacrifices to find the time and resources to do our health support work for which we are rarely compensated. A couple of boxes of free strips is not a trivial issue for many of us. A plane ticket may be out of reach. I have no doubt that we bloggers are highly ethical people, but the impact of the research suggests that drug and device company techniques work very well to influence ethical people who believe they are not being influenced.
Let's Come Up with Our Own Code of Ethics
In this post, I would like to open discussion to all bloggers, community leaders, and blog readers on the topic of what would be a responsible code of ethics for us NON health care providers who provide health information and health-related support to the online community.
For the purposes of this discussion I will define a new group of Online Health Support Providers (OHSP).
Here are my thoughts:
1. OHSP shall not accept any free or discounted items from any health-care related company that are not simultaneously offered free or discounted to the rest of the online community.
2. OHSP who agree to review a product or service shall review it honestly and shall provide reviews for ALL products or services they accept for review, not just those they can endorse.
3. OHSP who allow advertising on their web pages shall make it clear whether they select and endorse the products advertised on their pages. Because Google Ads are the only advertising vehicle available to most bloggers, bloggers who run Google Ads will indicate on their blog that they do NOT have the ability to control the ads that appear on their pages and that they do not endorse the products appearing in Google Ads. If informed by a blog viewer that an ad (with URL) running on their pages is abusive, OHSP agrees to investigate and if the ad is abusive to block the abusive ad via their Google Ads account.
4. OHSP have the right to report their personal experiences with any health related product or service and to highlight stories in the media or medical press relating to any product or service, however any relationship with the companies who produce these goods and services must be disclosed to readers following the same guidelines as are now required by medical journals. This includes disclosing any personal relationship in the past or present with the companies, including past employment, employment of relatives, or past sponsorships, consultancies, etc. OHSP will disclose any significant holdings in the stock of a company whose products they discuss.
5. OHSP who receive compensation for their blog posts from web sites owned by companies will disclose to their readers that they are paid bloggers and indicate who pays them.
This is just a start. I want to hear your suggestions and Ideas.
It turns out that the medical device manufacturing community's trade group, AdvaMed, proposed a Code of Ethics for its members in December 2008 which specifically banned all gifts or providing of entertainment to medical care providers.
AdvaMe is short for the Advanced Medical Technology Association, a trade group that claims its members "produce nearly 90 percent of the health care technology purchased annually in the United States and more than 50 percent purchased annually around the world."
Here's what's included in its new Code of Ethics:
An explicit prohibition on providing entertainment or recreation to Health Care Professionals (HCPs). The changes prohibit gifts of any type -- including all non-educational branded promotional items -- regardless of value.This Code of Ethics went into effect July 1, 2009.
Note that the code only applies to "health care providers." Not bloggers or those who maintain online support communities. Which might just have something to do with why a medical device maker is suddenly so interested in us humble bloggers.
Doctors are educated highly-paid professionals who, if anything, we would expect to be less influenced by small gifts and junkets, since they can well afford to spend their own money for such things. But it turns out small gifts have a subtle but very effective impact even on wealthy physicians.
You can read a good summary of research documenting how drug company gifts and junkets affect prescribing information in the following journal article. Follow the footnotes to find the studies summarized:
Do Drug Company Do drug company promotions influence physician behavior? Bob Goodman. West J Med.(BMJ) 2001 April; 174(4): 232–233.
How much more likely are we bloggers to be manipulated by drug and device companies?
Many of us earn very modest incomes or are retired. We make huge sacrifices to find the time and resources to do our health support work for which we are rarely compensated. A couple of boxes of free strips is not a trivial issue for many of us. A plane ticket may be out of reach. I have no doubt that we bloggers are highly ethical people, but the impact of the research suggests that drug and device company techniques work very well to influence ethical people who believe they are not being influenced.
Let's Come Up with Our Own Code of Ethics
In this post, I would like to open discussion to all bloggers, community leaders, and blog readers on the topic of what would be a responsible code of ethics for us NON health care providers who provide health information and health-related support to the online community.
For the purposes of this discussion I will define a new group of Online Health Support Providers (OHSP).
Here are my thoughts:
1. OHSP shall not accept any free or discounted items from any health-care related company that are not simultaneously offered free or discounted to the rest of the online community.
2. OHSP who agree to review a product or service shall review it honestly and shall provide reviews for ALL products or services they accept for review, not just those they can endorse.
3. OHSP who allow advertising on their web pages shall make it clear whether they select and endorse the products advertised on their pages. Because Google Ads are the only advertising vehicle available to most bloggers, bloggers who run Google Ads will indicate on their blog that they do NOT have the ability to control the ads that appear on their pages and that they do not endorse the products appearing in Google Ads. If informed by a blog viewer that an ad (with URL) running on their pages is abusive, OHSP agrees to investigate and if the ad is abusive to block the abusive ad via their Google Ads account.
4. OHSP have the right to report their personal experiences with any health related product or service and to highlight stories in the media or medical press relating to any product or service, however any relationship with the companies who produce these goods and services must be disclosed to readers following the same guidelines as are now required by medical journals. This includes disclosing any personal relationship in the past or present with the companies, including past employment, employment of relatives, or past sponsorships, consultancies, etc. OHSP will disclose any significant holdings in the stock of a company whose products they discuss.
5. OHSP who receive compensation for their blog posts from web sites owned by companies will disclose to their readers that they are paid bloggers and indicate who pays them.
This is just a start. I want to hear your suggestions and Ideas.
July 28, 2009
Clarification: Read Before You Flame
ADDED 7/31/09: Check out this blog post about how a huge health care charity, the AHA, co-opted bloggers to spread a "healthy message" while requiring them to avoid reporting on competitors AHA's sponsors Merck and Macy's.
Bloggers Can Spread the Word--Just Not About the Sponsors' Competitors
Now back to my original blog post:
I want to make something very clear: my point in the previous post was not that the people Roche identified as "influential bloggers" were sell outs. My point was that when a company like Roche decides as part of a marketing action to define who is influential in our community, everyone in the community needs to stop and think about what that means.
When I said we need to look at the posts of the people who went to this shindig my point was not that these people had sold out, but that because this was an attempt to co-opt leaders in a vibrant online community, we need to look at what happens next. Did it work? The blogs of these people would be the obvious place to look.
We know that drug companies have a long history of targeting and co-opting doctors who are considered influential. These efforts have been very successful. Not so incidentally, we are about to hear a lot more about the problems with meters, since the FDA is considering taking on the meter manufacturers and demanding they improve their meters' accuracy as there is solid evidence that meters meeting the currently defined woefully broad "acceptable" range of meter accuracy is killing people.
This topic was discussed recently in the NYTimes. I have already blogged about it. Did these other influential bloggers? I don't know. They each have their own area of focus and meter accuracy might not be relevant to the topics they cover. But with this issue emerging, what better time for Roche to build "partnerships" with the blogging community.
I know people like Scott Strumello--the very influential--and brilliant--blogger whose blog clued me into this story--are not about to stop reporting about drug company malfeasance no matter how many plane tickets Roche buys him.
I hope Scott will look into the question of what happened to the patents for all the non-invasive blood sugar meter patents that have been tested over the past decade, found to work well, and then disappeared forever. Usually this kind of product disappearance is a sign a large company has bought the patents to keep them from being used by competitors. Since meter companies make their money selling you strips at $1.07 a piece, a meter that does not use comsumables could destroy their cash cow and the price of buying the patent is nothing compared to lost profits. I think of this every time I use my blood pressure meter, for free.
I understand that some blogs are about reassuring people and reaching out and sharing compassionate friendship to people dealing with a very tough diagnosis. I do not suggest that isn't important. it is very important. If this meeting had been defined as a meeting of people with Type 1 who publish supportive blogs for other people with Type 1 diabetes I would have kept my mouth shut.
But it wasn't. It was described as a meeting of the top influential diabetes bloggers. A look at who was invited made it clear that it included Type 2s and that it included people who, like me, do not do compassionate outreach, but who review and endorse products for Type 2s. But it also stuck out that the people who were included who review product did not publish negative reviews about the random number generator Roche sent them this past winter, either. A salient point? Who knows. If nothing else, it is one worth some discussion.
This is why I raised the issue. Not as an attack on other bloggers but because in all the reports I read of the conference in the blogs of these other bloggers I did NOT see anyone raise the issue of what it means to let a company like Roche define who is influential. No one seems to have a problem, either, with the idea that Roche will decide which bloggers newly diagnosed people should be steered to by giving beautifully produced, glossy blog lists to doctors to distribute to newly diagnosed patients.
If I had been invited, I would have made the exact same points.
If you are invited to a subsequent get together or start receiving marketing materials from Roche--and trust me every communication you get from a company like Roche IS marketing material--give it some thought yourself.
The research on the impact of drug company marketing on doctors is that doctors, when asked, report that they aren't influenced by the meals, toys, classes, junkets etc. they get from drug and device companies, but that their prescribing patterns tell a very different story. That's why the drug and device companies do what they do. And if the are now moving to do it to us, we shouldn't expect to do any better than the doctors.
Bloggers Can Spread the Word--Just Not About the Sponsors' Competitors
Now back to my original blog post:
I want to make something very clear: my point in the previous post was not that the people Roche identified as "influential bloggers" were sell outs. My point was that when a company like Roche decides as part of a marketing action to define who is influential in our community, everyone in the community needs to stop and think about what that means.
When I said we need to look at the posts of the people who went to this shindig my point was not that these people had sold out, but that because this was an attempt to co-opt leaders in a vibrant online community, we need to look at what happens next. Did it work? The blogs of these people would be the obvious place to look.
We know that drug companies have a long history of targeting and co-opting doctors who are considered influential. These efforts have been very successful. Not so incidentally, we are about to hear a lot more about the problems with meters, since the FDA is considering taking on the meter manufacturers and demanding they improve their meters' accuracy as there is solid evidence that meters meeting the currently defined woefully broad "acceptable" range of meter accuracy is killing people.
This topic was discussed recently in the NYTimes. I have already blogged about it. Did these other influential bloggers? I don't know. They each have their own area of focus and meter accuracy might not be relevant to the topics they cover. But with this issue emerging, what better time for Roche to build "partnerships" with the blogging community.
I know people like Scott Strumello--the very influential--and brilliant--blogger whose blog clued me into this story--are not about to stop reporting about drug company malfeasance no matter how many plane tickets Roche buys him.
I hope Scott will look into the question of what happened to the patents for all the non-invasive blood sugar meter patents that have been tested over the past decade, found to work well, and then disappeared forever. Usually this kind of product disappearance is a sign a large company has bought the patents to keep them from being used by competitors. Since meter companies make their money selling you strips at $1.07 a piece, a meter that does not use comsumables could destroy their cash cow and the price of buying the patent is nothing compared to lost profits. I think of this every time I use my blood pressure meter, for free.
I understand that some blogs are about reassuring people and reaching out and sharing compassionate friendship to people dealing with a very tough diagnosis. I do not suggest that isn't important. it is very important. If this meeting had been defined as a meeting of people with Type 1 who publish supportive blogs for other people with Type 1 diabetes I would have kept my mouth shut.
But it wasn't. It was described as a meeting of the top influential diabetes bloggers. A look at who was invited made it clear that it included Type 2s and that it included people who, like me, do not do compassionate outreach, but who review and endorse products for Type 2s. But it also stuck out that the people who were included who review product did not publish negative reviews about the random number generator Roche sent them this past winter, either. A salient point? Who knows. If nothing else, it is one worth some discussion.
This is why I raised the issue. Not as an attack on other bloggers but because in all the reports I read of the conference in the blogs of these other bloggers I did NOT see anyone raise the issue of what it means to let a company like Roche define who is influential. No one seems to have a problem, either, with the idea that Roche will decide which bloggers newly diagnosed people should be steered to by giving beautifully produced, glossy blog lists to doctors to distribute to newly diagnosed patients.
If I had been invited, I would have made the exact same points.
If you are invited to a subsequent get together or start receiving marketing materials from Roche--and trust me every communication you get from a company like Roche IS marketing material--give it some thought yourself.
The research on the impact of drug company marketing on doctors is that doctors, when asked, report that they aren't influenced by the meals, toys, classes, junkets etc. they get from drug and device companies, but that their prescribing patterns tell a very different story. That's why the drug and device companies do what they do. And if the are now moving to do it to us, we shouldn't expect to do any better than the doctors.
It's Official: I'm Not An Influential Blogger
With much ballyhoo Roche just flew what they defined as the 29 most "influential" diabetes bloggers to an all expenses paid talk fest where, it appears, everything diabetes was open to discussion except the price of test strips and the inaccuracy of meters. Roche, in case you forgot, is the company that manufactures the Accu-Chek Aviva meter.
I recognized many of the attendees, who are indeed influential. But by no means all. In fact there were seven "influential" bloggers I had never before heard of including a recently diagnosed person with Type 2 who according to Google Reader has a whopping 38 subscribers.
Roche stated that they intend to publish materials for the newly diagnosed that will point them to these chosen people's blogs, which makes it more than an issue of wounded pride to me that this blog and its associated Blood Sugar 101 blog were ignored.
I have a lot more than 38 subscribers on Google News, folks. My latest Google Analytics report says that over the past month some 65,000 people visited my pages of whom almost 10,000 are returning visitors. Google makes these statistics available to advertisers. They aren't kept secret. I know for a fact that quite a few of the "influential bloggers" are not drawing anywhere near that kind of traffic and, in the case of the diabetes community sites invited, their retention levels--returning visitors month by month--are far lower than my 10,000.
So it does not take advanced paranoia to wonder if the reason I was excluded was that I blogged several times about the egregiously poor performance of Roche's Aviva meter. I have had three of them and all three were dangerously inaccurate, not matching lab results, and more importantly, not matching the meter's own results on closely repeated tests with the same blood draw.
Since the influential diabetes bloggers who were invited report that Roche's reps made it clear that opening a discussion about problems with their meters and strips were offensive, the reasons for my exclusion are clear.
Unfortunately, though, my exclusion means that Roche will finance the production of materials that doctors will give to the newly diagnosed pointing them to blogs full of feel-good posts about living with diabetes, enthusiastic endorsements of products the blogger has gotten for free, and no pointers to the vital information that could keep them from developing diabetic complications.
Because folks, whatever else you read on these pages, the central mission of this blog and the Blood Sugar 101 web site, is to let people know the truth about what blood sugar levels destroy their bodies and what the safe and effective strategies are that they can use to avoid this damage.
This message works. I hear on a regular basis from people who tell me they followed the advice given on the page about How To Get Your Blood Sugar Under Control and brought their A1cs down into the 5% range, even when they started with A1cs as high as 15%. And it isn't just the newly diagnosed. I heard recently heard from someone who brought a 15% A1c down into the normal range with these techniques who was a decade past diagnosis.
So Roche's decision to choose "feel good" diabetes bloggers as representatives of the "online diabetes community" and omit these pages from its list of recommended sites intended to be distributed to all newly diagnosed people with diabetes is not trivial.
It will also mean more people with Type 2 who blame themselves for causing their diabetes will not learn the truth about the real causes of Type 2 Diabetes. Blaming people for causing their Type 2 diabetes is a tragic trend, promoted by the media and all too many doctors.
Why is it tragic? Because guilt and self-hatred leads to denial. I cannot tell you how many people I have heard from who told me that until they learned that they did NOT cause their Type 2 diabetes by reckless overeating they could not bear to do the research it would take to conquer it. I have even heard a truly devastating story--from a local acquaintance--about a woman in her early 50s who refused a kidney transplant because she believed she had caused her diabetes and decided she didn't deserve the kidney.
Beyond that, Roche's move to define and support their choice of "influential diabetes bloggers" and to promote their selection of these bloggesr to the media should be a warning to all of us.
It illuminates the strategies used to control discourse that are employed by the commercial interests that profit mightily by exploiting those of us with diabetes of every type.
If they can't silence the bloggers who tell the truths that don't support their profits they can anoint other, less threatening bloggers, give them a high profile, and hope that by doing so they can herd the newly diagnosed people to bloggers who won't keep them from buying their inaccurate overpriced meters, expensive dangerous drugs, and deceptively promoted high carb "healthy" foods marketed by greedy corporations.
Because it's a simple fact, known to everyone in marketing, that if you give people free air fare, free premium hotel rooms, and expensive meals, they will think twice about attacking your products. That is why drug companies wine and and dine doctors. Because it works. It is why Roche flew in all these influential diabetes bloggers and laid out the high price spread for them.
Keep an eye on these "influential bloggers" over the next month and track how many mention the FDA's attempt to demand accountability from meter manufacturers. Track how many report research about the dangers of the drugs being forced on people with diabetes. Compare the ratio of feel good/cat blogging on their pages to information that might prevent one person from coming down with an unnecessary diabetic complication.
And if telling the truth will keep me from being "influential" as defined by meter companies, drug companies and the ADA, I'm just going to have to live with it. And console myself with the rate my blog traffic is growing at, which is currently a healthy 50% a year.
I recognized many of the attendees, who are indeed influential. But by no means all. In fact there were seven "influential" bloggers I had never before heard of including a recently diagnosed person with Type 2 who according to Google Reader has a whopping 38 subscribers.
Roche stated that they intend to publish materials for the newly diagnosed that will point them to these chosen people's blogs, which makes it more than an issue of wounded pride to me that this blog and its associated Blood Sugar 101 blog were ignored.
I have a lot more than 38 subscribers on Google News, folks. My latest Google Analytics report says that over the past month some 65,000 people visited my pages of whom almost 10,000 are returning visitors. Google makes these statistics available to advertisers. They aren't kept secret. I know for a fact that quite a few of the "influential bloggers" are not drawing anywhere near that kind of traffic and, in the case of the diabetes community sites invited, their retention levels--returning visitors month by month--are far lower than my 10,000.
So it does not take advanced paranoia to wonder if the reason I was excluded was that I blogged several times about the egregiously poor performance of Roche's Aviva meter. I have had three of them and all three were dangerously inaccurate, not matching lab results, and more importantly, not matching the meter's own results on closely repeated tests with the same blood draw.
Since the influential diabetes bloggers who were invited report that Roche's reps made it clear that opening a discussion about problems with their meters and strips were offensive, the reasons for my exclusion are clear.
Unfortunately, though, my exclusion means that Roche will finance the production of materials that doctors will give to the newly diagnosed pointing them to blogs full of feel-good posts about living with diabetes, enthusiastic endorsements of products the blogger has gotten for free, and no pointers to the vital information that could keep them from developing diabetic complications.
Because folks, whatever else you read on these pages, the central mission of this blog and the Blood Sugar 101 web site, is to let people know the truth about what blood sugar levels destroy their bodies and what the safe and effective strategies are that they can use to avoid this damage.
This message works. I hear on a regular basis from people who tell me they followed the advice given on the page about How To Get Your Blood Sugar Under Control and brought their A1cs down into the 5% range, even when they started with A1cs as high as 15%. And it isn't just the newly diagnosed. I heard recently heard from someone who brought a 15% A1c down into the normal range with these techniques who was a decade past diagnosis.
So Roche's decision to choose "feel good" diabetes bloggers as representatives of the "online diabetes community" and omit these pages from its list of recommended sites intended to be distributed to all newly diagnosed people with diabetes is not trivial.
It will also mean more people with Type 2 who blame themselves for causing their diabetes will not learn the truth about the real causes of Type 2 Diabetes. Blaming people for causing their Type 2 diabetes is a tragic trend, promoted by the media and all too many doctors.
Why is it tragic? Because guilt and self-hatred leads to denial. I cannot tell you how many people I have heard from who told me that until they learned that they did NOT cause their Type 2 diabetes by reckless overeating they could not bear to do the research it would take to conquer it. I have even heard a truly devastating story--from a local acquaintance--about a woman in her early 50s who refused a kidney transplant because she believed she had caused her diabetes and decided she didn't deserve the kidney.
Beyond that, Roche's move to define and support their choice of "influential diabetes bloggers" and to promote their selection of these bloggesr to the media should be a warning to all of us.
It illuminates the strategies used to control discourse that are employed by the commercial interests that profit mightily by exploiting those of us with diabetes of every type.
If they can't silence the bloggers who tell the truths that don't support their profits they can anoint other, less threatening bloggers, give them a high profile, and hope that by doing so they can herd the newly diagnosed people to bloggers who won't keep them from buying their inaccurate overpriced meters, expensive dangerous drugs, and deceptively promoted high carb "healthy" foods marketed by greedy corporations.
Because it's a simple fact, known to everyone in marketing, that if you give people free air fare, free premium hotel rooms, and expensive meals, they will think twice about attacking your products. That is why drug companies wine and and dine doctors. Because it works. It is why Roche flew in all these influential diabetes bloggers and laid out the high price spread for them.
Keep an eye on these "influential bloggers" over the next month and track how many mention the FDA's attempt to demand accountability from meter manufacturers. Track how many report research about the dangers of the drugs being forced on people with diabetes. Compare the ratio of feel good/cat blogging on their pages to information that might prevent one person from coming down with an unnecessary diabetic complication.
And if telling the truth will keep me from being "influential" as defined by meter companies, drug companies and the ADA, I'm just going to have to live with it. And console myself with the rate my blog traffic is growing at, which is currently a healthy 50% a year.
July 24, 2009
Phosphates in "Enhanced" Supermarket Meats
When we cut the carbs, a lot of use end up eating more meat. I have debunked quite a few poorly conducted studies that pretend to prove that eating meat raises mortality.
But a recent study raises an issue about meat that is important to people with diabetes.
Science Daily: Fresh Meats Often Contain Additives Harmful to Dialysis Patients
Supermarkets sell in the fresh meat department meats they label as "enhanced." These are meats that have been injected with solutions that are supposed to "enhance flavor" though of course, since they are mostly water, what they really do is enhance weight, allowing the supermarket to charge you more for the same piece of meat, since it has gained a couple ounces from being injected.
The study found that these enhanced meats contain levels of phosphate much higher than found in untreated meat. This can be extremely harmful to people on dialysis.
What the study did not mention is that phosphates can also be harmful to everyone else. Lifetime phosphate intake has been linked to the likelihood of developing kidney disease in everyone, not just people with diabetes.
I blogged about this a while ago here:
Coke Adds Death
and more recently here:
Avoid Phosphates and Preserve Your Kidneys
This research also points out that the labels on treated meat do not reveal the ingredients. My guess is that besides the phosphates, which were identified via lab analysis, these "enhanced" meats are also filled with MSG which, among other things, dysregulates appetite and contributes to weight gain.
Let your supermarket manager know that the store is selling a product that contains a dangerous chemical that could kill people on dialysis and which is NOT labeled to indicate this. Fear of lawsuits is a strong motivator for change. It's time that meat labels contained the same level of disclosure we find on other supermarket foods. Without disclosure we cannot know that what we are eating is not adulterated.
But a recent study raises an issue about meat that is important to people with diabetes.
Science Daily: Fresh Meats Often Contain Additives Harmful to Dialysis Patients
Supermarkets sell in the fresh meat department meats they label as "enhanced." These are meats that have been injected with solutions that are supposed to "enhance flavor" though of course, since they are mostly water, what they really do is enhance weight, allowing the supermarket to charge you more for the same piece of meat, since it has gained a couple ounces from being injected.
The study found that these enhanced meats contain levels of phosphate much higher than found in untreated meat. This can be extremely harmful to people on dialysis.
What the study did not mention is that phosphates can also be harmful to everyone else. Lifetime phosphate intake has been linked to the likelihood of developing kidney disease in everyone, not just people with diabetes.
I blogged about this a while ago here:
Coke Adds Death
and more recently here:
Avoid Phosphates and Preserve Your Kidneys
This research also points out that the labels on treated meat do not reveal the ingredients. My guess is that besides the phosphates, which were identified via lab analysis, these "enhanced" meats are also filled with MSG which, among other things, dysregulates appetite and contributes to weight gain.
Let your supermarket manager know that the store is selling a product that contains a dangerous chemical that could kill people on dialysis and which is NOT labeled to indicate this. Fear of lawsuits is a strong motivator for change. It's time that meat labels contained the same level of disclosure we find on other supermarket foods. Without disclosure we cannot know that what we are eating is not adulterated.
July 22, 2009
Bad Science: Does Metformin Inhibit DPP-4?
A study in the news a few weeks ago purports to show that Metformin inhibits DPP-4, the protease that cleaves GLP-1. If this were true, it would be a major concern to people with diabetes, because DPP-4 is a known tumor suppressor and inhibiting it increases the likelihood that cancerous cells will proliferate without being destroyed by the immune system. Since the study also found that this supposed effect was suppressed when metformin was taken along with a meal, you might think I was going to suggest you protect yourself by not taking metformin in the fasting state.
But that would be only if I hadn't reviewed the study, which breaks new ground for published awfulness. In fact, I've seen better designed research presented at Junior High School science fairs.
Here's the abstract of the study.
Investigation of the effect of oral metformin on dipeptidylpeptidase-4 (DPP-4) activity in Type 2 diabetes. Cuthbertson, et al. Diabetic Medicine Volume 26, Number 6, June 2009 , pp. 649-654(6)
I don't have access to the full text, and neither does Diabetes in Control, which reported on this study, citing only the information in the abstract. But what a train wreck of an abstract it is!
The entire methods section is this:
Note also that there is no explanation of what was measured in these subjects, when it was measured, or, for that matter, why.
The "Results" section is not much more informative. The researchers report that:
As far as I can figure from this extremely poorly written abstract the finding the researchers and peer reviewers considered worthy of publication was a 5% difference in an average of some undefined "Area Under the Curve" between the larger group--which ate a meal with their metformin and a subgroup which took metformin fasting.
Did they assess DPP-4 "activity" by working statistical magic on some mix of measured GLP-1 levels, insulin levels and glucose levels which are what they mention measuring? If so, you would want to ask yourself why this would be a meaningful measure of "DPP-4 activity?" There may well be other factors that affect GLP-1 levels, insulin, and glucose that have nothing to do with DPP-4, and indeed there are.
They also note that "Metformin serum levels were significantly lower (P < 0.001) after SMM than fasting (AUC0-4 h 350 ± 66 vs. 457 ± 55 mg/ml/min)," though what this is supposed to mean in relation to their other reported findings is completely unexplained.
But it really doesn't matter what these researchers report, because, folks, when you are comparing an average of a measurement taken in a group of 10 people to an average of a measurement taken in 6 people who form a subset of that original 10 people, you can run all the statistical software you want, and come out with numbers to ten places of significance, but your result is still junk.
Your sample size is too small to yield averages that eliminate the impact of individual variations.
To understand this better consider this hypothetical example: Let's say you are studying whether eating cheese sandwiches for lunch makes people wealthy. You start with ten people, five of whom are corporate executives and five of whom are janitors.
You feed them something other than a cheese sandwich for one lunch and average their income over the next month. The next month you call back six of the original ten subjects, randomly chosen, and end up with a subgroup where five are corporate executives and one is a janitor. You feed them cheese sandwiches for lunch, and by golly, a month later you see a dramatic difference in average income between the two groups. Have you proven that eating cheese sandwiches for lunch raises income? Of course not.
Your "result" here is caused entirely by differences between the larger and smaller group which become more significant because the group was so tiny to start with and you've reduced it to a size where two or three people's individual variations can have a huge impact on your average. In the metformin study the "finding" is a difference of 5% between the two groups, a difference in an average no less, which makes it statistically significant only if you ignore everything but the results displayed by your statistical software which is too polite to tell you that only an imbecile would run statistics in this kind of situation.
In fact, the result in the smaller, fasting subgroup which is what the researchers considered worth a journal publication may differ because that group may have selected, from the original group, more people with high natural GLP-1--or lower DPP-4--production. The second subgroup may have had different average insulin producing capability. There might be differences in the degree to which the subjects digest metformin. There may be differences in their body size which affects all these parameters. There may be huge differences in how responsive their livers are to metformin. With the study design here, we will never know.
But the main point is that with a tiny study population like this one, if you compare any average measurement made in the total group to a measurement taken in a significantly smaller subgroup, any result is junk.
And that doesn't even get into the question of what did this study do to determine that inhibition of DPP-4 was what produced its reported result, if that result were, miraculously, not a statistical artifact.
So this study tells us nothing about whether metformin inhibits DPP-4 and whether this effect is wiped out by administering metformin with food.
In case you wonder if there is any research on this subject that is more useful, here's an old study that looked at this question in a more scientific way:
Metformin effects on dipeptidylpeptidase IV degradation of glucagon-like peptide-1. Hinke SA et al. Biochem Biophys Res Commun. 2002 Mar 15;291(5):1302-8.
Note that this old study cites other studies that have found that Metformin increases GLP-1, so it is quite possible it does. But there is no reason to believe that GLP-1 is only increased by inhibiting DPP-4. It is quite possible you could increase GLP-1 by doing something to stimulate the secretion of GLP-1 for a longer time period after eating. And it's worth noting that this older second study could not find any evidence that, based on sophisticated in vitro examination, metformin had the biochemical ability to inhibit DPP-4.
But that would be only if I hadn't reviewed the study, which breaks new ground for published awfulness. In fact, I've seen better designed research presented at Junior High School science fairs.
Here's the abstract of the study.
Investigation of the effect of oral metformin on dipeptidylpeptidase-4 (DPP-4) activity in Type 2 diabetes. Cuthbertson, et al. Diabetic Medicine Volume 26, Number 6, June 2009 , pp. 649-654(6)
I don't have access to the full text, and neither does Diabetes in Control, which reported on this study, citing only the information in the abstract. But what a train wreck of an abstract it is!
The entire methods section is this:
Ten subjects with Type 2 diabetes (6 male/4 female, age 65.8 ± 2.6 years, body mass index 30.0 ± 1.2 kg/m2, glycated haemoglobin (HbA1c) 6.3 ± 0.2%, mean ± sem) received metformin 1 g orally or placebo together with a standard mixed meal (SMM) in a random crossover design. Six subjects re-attended fasting and received metformin 1 g without a SMM. [Emphasis mine]They start with a whopping ten subjects and then compare them to a subgroup of six subjects taken from the original group of ten. Note that the metformin was taken with the meal first and then fasting second. There is no indication if these subjects were on metformin before the study or if these were the the first doses of metformin these subjects had taken. This is significant as metformin's impact increases with each dose a naive user takes and it takes about a week to start showing many of its physiological effects.
Note also that there is no explanation of what was measured in these subjects, when it was measured, or, for that matter, why.
The "Results" section is not much more informative. The researchers report that:
DPP-4 activity was not suppressed by metformin compared with placebo [area under curve (AUC)0-4 h 1574 ± 4 vs. 1581 ± 8 μmol/ml/min, respectively]. Plasma glucose, insulin and active GLP-1 were not different. However, DPP-4 activity was suppressed with metformin following fasting compared with a SMM (n = 6) (AUC0-4 h 1578 ± 4 vs. 1494 ± 9 μmol/min, P < 0.02). "Ahem, AUC0-4 h of what? "DPP-4 Activity" is not something you measure with a blood draw. DPP-4 concentration would be, but not activity. And since "DPP-4 activity" is defined nowhere in this abstract we are left scratching our heads as to what exactly they measured. And what "placebo" are they talking about? I don't see a placebo described anywhere in the methods section.
As far as I can figure from this extremely poorly written abstract the finding the researchers and peer reviewers considered worthy of publication was a 5% difference in an average of some undefined "Area Under the Curve" between the larger group--which ate a meal with their metformin and a subgroup which took metformin fasting.
Did they assess DPP-4 "activity" by working statistical magic on some mix of measured GLP-1 levels, insulin levels and glucose levels which are what they mention measuring? If so, you would want to ask yourself why this would be a meaningful measure of "DPP-4 activity?" There may well be other factors that affect GLP-1 levels, insulin, and glucose that have nothing to do with DPP-4, and indeed there are.
They also note that "Metformin serum levels were significantly lower (P < 0.001) after SMM than fasting (AUC0-4 h 350 ± 66 vs. 457 ± 55 mg/ml/min)," though what this is supposed to mean in relation to their other reported findings is completely unexplained.
But it really doesn't matter what these researchers report, because, folks, when you are comparing an average of a measurement taken in a group of 10 people to an average of a measurement taken in 6 people who form a subset of that original 10 people, you can run all the statistical software you want, and come out with numbers to ten places of significance, but your result is still junk.
Your sample size is too small to yield averages that eliminate the impact of individual variations.
To understand this better consider this hypothetical example: Let's say you are studying whether eating cheese sandwiches for lunch makes people wealthy. You start with ten people, five of whom are corporate executives and five of whom are janitors.
You feed them something other than a cheese sandwich for one lunch and average their income over the next month. The next month you call back six of the original ten subjects, randomly chosen, and end up with a subgroup where five are corporate executives and one is a janitor. You feed them cheese sandwiches for lunch, and by golly, a month later you see a dramatic difference in average income between the two groups. Have you proven that eating cheese sandwiches for lunch raises income? Of course not.
Your "result" here is caused entirely by differences between the larger and smaller group which become more significant because the group was so tiny to start with and you've reduced it to a size where two or three people's individual variations can have a huge impact on your average. In the metformin study the "finding" is a difference of 5% between the two groups, a difference in an average no less, which makes it statistically significant only if you ignore everything but the results displayed by your statistical software which is too polite to tell you that only an imbecile would run statistics in this kind of situation.
In fact, the result in the smaller, fasting subgroup which is what the researchers considered worth a journal publication may differ because that group may have selected, from the original group, more people with high natural GLP-1--or lower DPP-4--production. The second subgroup may have had different average insulin producing capability. There might be differences in the degree to which the subjects digest metformin. There may be differences in their body size which affects all these parameters. There may be huge differences in how responsive their livers are to metformin. With the study design here, we will never know.
But the main point is that with a tiny study population like this one, if you compare any average measurement made in the total group to a measurement taken in a significantly smaller subgroup, any result is junk.
And that doesn't even get into the question of what did this study do to determine that inhibition of DPP-4 was what produced its reported result, if that result were, miraculously, not a statistical artifact.
So this study tells us nothing about whether metformin inhibits DPP-4 and whether this effect is wiped out by administering metformin with food.
In case you wonder if there is any research on this subject that is more useful, here's an old study that looked at this question in a more scientific way:
Metformin effects on dipeptidylpeptidase IV degradation of glucagon-like peptide-1. Hinke SA et al. Biochem Biophys Res Commun. 2002 Mar 15;291(5):1302-8.
Note that this old study cites other studies that have found that Metformin increases GLP-1, so it is quite possible it does. But there is no reason to believe that GLP-1 is only increased by inhibiting DPP-4. It is quite possible you could increase GLP-1 by doing something to stimulate the secretion of GLP-1 for a longer time period after eating. And it's worth noting that this older second study could not find any evidence that, based on sophisticated in vitro examination, metformin had the biochemical ability to inhibit DPP-4.
July 20, 2009
The FDA Notices Meter Inaccuracy
Here's some evidence that "change" is more than a campaign slogan. After eight years when the FDA behaved like a wholly owned subsidiary of the drug industry, there are small signs that the incoming leadership might use its power to help patients, rather than those who prey on them.
I'm referring of course to the report published in the New York Times this weekend that the FDA is considering taking steps to do something to remedy the abysmal accuracy of the blood sugar meters sold to the public.
You can read the report here:
Standards Might Rise on Monitors for Diabetics
What other high tech product can you think of where the markup on the manufacturing cost is in the 10,000% range while well conducted research has proven that the accuracy can be off by as much as 32%?
The drug companies who sell us these obscenely expensive and highly inaccurate devices cover themselves by stating they meet an international standard. What they don't tell you is who set that standard and who ensures it doesn't change. Three guesses and the first two don't count.
Now the FDA is suggesting that it will publish its own standard if the international standard setting body doesn't act to tighten the accuracy standard from its current abysmally wide setting. The government is a huge customer for blood sugar meters, since so many of them are sold to Medicare patients, so if the FDA were to set a new, tighter, standard it would impel meter makers to improve the woeful performance of their products.
I've been using a meter for just shy of 11 years. The Aviva meter I tried and threw out last winter was no more accurate than the ExacTech brand meter I started out with in 1998. In fact, given the wide variation from reading to reading, the Aviva may have been worse. The 2009 Aviva varied from the 1998 meter in three particulars. It took a lot less blood to get a reading, the reading appeared faster, and the strips cost $1.07 apiece retail where the ExacTech strips had cost about $.40 each.
I have long questioned why the huge "charitable" organizations that collect money in the name of people with diabetes have kept silent on this issue. But you have only to look at the ads from meter companies in the publications of organizations like the ADA and JDRF to get your answer. These "sponsors" are cash cows for these organizations, so they are not about to challenge them, even though as the NYTimes article points out, meter manufacturers' greed and resistance to improving their products' quality is not only beggaring people with diabetes, it is killing them.
The NYTimes article points out something I hadn't known: A major difference between the recent study that found that keeping blood sugar tightly controlled in the ICU preserved lives and the one that found that keeping tight control in the ICU caused more deaths was this: the first study used a highly accurate blood sugar meter available only to hospitals. The other used the crappy meters and strips you and I are paying all that money for each month.
When a meter is off by 32% it is impossible to use it to achieve tight control because a reading of 80 mg/dl, a safe, normal number might actually represent a blood sugar level of 54 mg/dl which is very far from safe--especially if it is heading down.
I learned this the hard way a few years ago. When I started insulin I went out and got a brand new meter--an Aviva since I understood that using insulin would require that my readings be as accurate as possible. Since my doctor thought, incorrectly, that I was a "classic Type 2" he started me at a much higher insulin dose than would have been right for me. I developed the classic symptoms of hypo--pounding pulse, waking from sleep at 4AM in a cold sweat, but my meter readings were in the normal range. It was only when I took my meter to the lab and tested within a minute of the blood draw that I learned that my shiny new meter was giving a result that was over 40 mg/dl higher than the lab reading. That was a post-meal test where I was tested with a high blood sugar since my doctor was questioning that I needed insulin and I had to demonstrate why. But given the 40 mg/dl accuracy gap I saw with a reading over 200 mg/dl, who knows what the 90s my bright shiny new Aviva meter was spitting out--to the tune of over $1 a test--really were?
When I contacted Roche, the Aviva's manufacturer, to complain about the poor performance of my Aviva, the customer rep assured me that the reading was "within the accepted standard" which, since I knew what the standard was, I knew wasn't true.
The rep immediately transferred me to someone who tried to get met to say, on a recorded line, that I had not been harmed by the inaccurate meter reading--at the same time that the company was protesting that the meter reading was within an acceptable range of accuracy. When I refused I was transferred to yet another company operative who tried to force me to make the statement exonerating the company.
The company's priorities were crystal clear. That I ended up with three doctor visits trying to find the cause for my nonstop high pulse was seen only as a threat to company profits.
I was using only 1/2 the dose of insulin my doctor had prescribed because I doubted I was a Type 2. If I had been less knowledgeable about diabetes and had started out with the full dose the doctor prescribed, I might well have ended up unconscious, or worse, with a blood sugar meter reading that would have given little clue as to why.
I was lucky, but as the NYTimes article makes clear, many others aren't. And even more people with diabetes decide it is foolish to pay $1.07 for test strips whose results may be so inaccurate as to be worthless. Since it is extremely difficult to maintain normal health if you don't keep track of what your blood sugar level is, this is another way that poor meter quality harms people with diabetes.
It this concerns you, drop a line to the FDA explaining that you are a consumer who uses a blood sugar meter and that you are sick of paying an exorbitant price for a product so inaccurate it may cause you serious health problems. Demand that the FDA stand up to the meter companies and tighten the standards for blood sugar meters.
The Ombudsman for the Center for Devices and Radiological Heath might be one place to start: ombudsman@cdrh.fda.gov.
The press officer for FDA regulation of devices is:
mary.long@fda.hhs.gov (Peper Long, according to the FDA Contact information page).
Finally, to save myself answering a LOT of email here are my current recommendations for blood sugar meters. Though they have poor accuracy, some meters are better than others, and using those meters properly can make a huge difference in your health. The email I receive from readers month after month suggests that using a meter can drop your A1c from as high as 14% to the 5% range. I often hear from people who have done just that using the technique described HERE. Even with an accuracy gap of 25%, a reading of 100 mg/dl is a lot better for your long-term health than one of 300 mg/dl.
I use an Ultra Mini, which is the most consistent meter I could find. It isn't perfect by any means, but it agrees with itself and with another, older Ultra I own pretty well. I have discarded my Ultra II which was not as consistent.
I recommend the Wal-mart Relion meter to people who are paying for their own strips as the Relion strips are much more affordable. The Relion strips are okay as long as you use them within a short period of opening the vial. Over time they seem to lose their accuracy.
If you are just starting blood sugar testing, don't panic if you see an unusual reading. Wash your hands, dry them, and test again to make sure that you didn't just get a bad strip. There are bad strips out there. Lots of them. Let's hope the FDA moves swiftly on this issue.
I'm referring of course to the report published in the New York Times this weekend that the FDA is considering taking steps to do something to remedy the abysmal accuracy of the blood sugar meters sold to the public.
You can read the report here:
Standards Might Rise on Monitors for Diabetics
What other high tech product can you think of where the markup on the manufacturing cost is in the 10,000% range while well conducted research has proven that the accuracy can be off by as much as 32%?
The drug companies who sell us these obscenely expensive and highly inaccurate devices cover themselves by stating they meet an international standard. What they don't tell you is who set that standard and who ensures it doesn't change. Three guesses and the first two don't count.
Now the FDA is suggesting that it will publish its own standard if the international standard setting body doesn't act to tighten the accuracy standard from its current abysmally wide setting. The government is a huge customer for blood sugar meters, since so many of them are sold to Medicare patients, so if the FDA were to set a new, tighter, standard it would impel meter makers to improve the woeful performance of their products.
I've been using a meter for just shy of 11 years. The Aviva meter I tried and threw out last winter was no more accurate than the ExacTech brand meter I started out with in 1998. In fact, given the wide variation from reading to reading, the Aviva may have been worse. The 2009 Aviva varied from the 1998 meter in three particulars. It took a lot less blood to get a reading, the reading appeared faster, and the strips cost $1.07 apiece retail where the ExacTech strips had cost about $.40 each.
I have long questioned why the huge "charitable" organizations that collect money in the name of people with diabetes have kept silent on this issue. But you have only to look at the ads from meter companies in the publications of organizations like the ADA and JDRF to get your answer. These "sponsors" are cash cows for these organizations, so they are not about to challenge them, even though as the NYTimes article points out, meter manufacturers' greed and resistance to improving their products' quality is not only beggaring people with diabetes, it is killing them.
The NYTimes article points out something I hadn't known: A major difference between the recent study that found that keeping blood sugar tightly controlled in the ICU preserved lives and the one that found that keeping tight control in the ICU caused more deaths was this: the first study used a highly accurate blood sugar meter available only to hospitals. The other used the crappy meters and strips you and I are paying all that money for each month.
When a meter is off by 32% it is impossible to use it to achieve tight control because a reading of 80 mg/dl, a safe, normal number might actually represent a blood sugar level of 54 mg/dl which is very far from safe--especially if it is heading down.
I learned this the hard way a few years ago. When I started insulin I went out and got a brand new meter--an Aviva since I understood that using insulin would require that my readings be as accurate as possible. Since my doctor thought, incorrectly, that I was a "classic Type 2" he started me at a much higher insulin dose than would have been right for me. I developed the classic symptoms of hypo--pounding pulse, waking from sleep at 4AM in a cold sweat, but my meter readings were in the normal range. It was only when I took my meter to the lab and tested within a minute of the blood draw that I learned that my shiny new meter was giving a result that was over 40 mg/dl higher than the lab reading. That was a post-meal test where I was tested with a high blood sugar since my doctor was questioning that I needed insulin and I had to demonstrate why. But given the 40 mg/dl accuracy gap I saw with a reading over 200 mg/dl, who knows what the 90s my bright shiny new Aviva meter was spitting out--to the tune of over $1 a test--really were?
When I contacted Roche, the Aviva's manufacturer, to complain about the poor performance of my Aviva, the customer rep assured me that the reading was "within the accepted standard" which, since I knew what the standard was, I knew wasn't true.
The rep immediately transferred me to someone who tried to get met to say, on a recorded line, that I had not been harmed by the inaccurate meter reading--at the same time that the company was protesting that the meter reading was within an acceptable range of accuracy. When I refused I was transferred to yet another company operative who tried to force me to make the statement exonerating the company.
The company's priorities were crystal clear. That I ended up with three doctor visits trying to find the cause for my nonstop high pulse was seen only as a threat to company profits.
I was using only 1/2 the dose of insulin my doctor had prescribed because I doubted I was a Type 2. If I had been less knowledgeable about diabetes and had started out with the full dose the doctor prescribed, I might well have ended up unconscious, or worse, with a blood sugar meter reading that would have given little clue as to why.
I was lucky, but as the NYTimes article makes clear, many others aren't. And even more people with diabetes decide it is foolish to pay $1.07 for test strips whose results may be so inaccurate as to be worthless. Since it is extremely difficult to maintain normal health if you don't keep track of what your blood sugar level is, this is another way that poor meter quality harms people with diabetes.
It this concerns you, drop a line to the FDA explaining that you are a consumer who uses a blood sugar meter and that you are sick of paying an exorbitant price for a product so inaccurate it may cause you serious health problems. Demand that the FDA stand up to the meter companies and tighten the standards for blood sugar meters.
The Ombudsman for the Center for Devices and Radiological Heath might be one place to start: ombudsman@cdrh.fda.gov.
The press officer for FDA regulation of devices is:
mary.long@fda.hhs.gov (Peper Long, according to the FDA Contact information page).
Finally, to save myself answering a LOT of email here are my current recommendations for blood sugar meters. Though they have poor accuracy, some meters are better than others, and using those meters properly can make a huge difference in your health. The email I receive from readers month after month suggests that using a meter can drop your A1c from as high as 14% to the 5% range. I often hear from people who have done just that using the technique described HERE. Even with an accuracy gap of 25%, a reading of 100 mg/dl is a lot better for your long-term health than one of 300 mg/dl.
I use an Ultra Mini, which is the most consistent meter I could find. It isn't perfect by any means, but it agrees with itself and with another, older Ultra I own pretty well. I have discarded my Ultra II which was not as consistent.
I recommend the Wal-mart Relion meter to people who are paying for their own strips as the Relion strips are much more affordable. The Relion strips are okay as long as you use them within a short period of opening the vial. Over time they seem to lose their accuracy.
If you are just starting blood sugar testing, don't panic if you see an unusual reading. Wash your hands, dry them, and test again to make sure that you didn't just get a bad strip. There are bad strips out there. Lots of them. Let's hope the FDA moves swiftly on this issue.
July 17, 2009
Very Bad Science: Nitrates Cause Type 2 Diabetes
As my readers know, after reading a lot of research I've become convinced that toxic pollutants in our environment are a major explanation for the growth of obesity and the rise of Type 2 diagnoses over the past decades.
So you might expect when reports appeared all over the media recently, linking the increase in diabetes to nitrates in our food, I would have welcomed it as yet another factor pointing to an environmental cause for diabetes.
I might have, had I not read a detailed description of the research in question. Unfortunately, this study turns out to be yet another example of faith-based research--research that interprets correlations as causation. That is, researchers determine that two things happen at the same time and conclude one must have caused the other. As is often the case, this kind of conclusion is based not on hard scientific fact but on the fact that the correlation supports a a religious belief: "Meat and fast foods are evil."
Only the abstract of the study is available for free, here:
Epidemiological Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer's Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis . Journal of Alzheimer's Disease,Suzanne M. de la Monte et al., Volume 17, Number 3 / 2009. doi: 10.3233/JAD-2009-1070
But fortunately, a news report gives the salient details of this study. You can read it here:
Medical News Today: Researchers Find Possible Environmental Causes For Alzheimer's, Diabetes
To explain why this study is so flawed you need to know something about what has made other studies linking environmental substances to diabetes so compelling. In those studies, researchers take a group of people who developed diabetes and look for hard evidence that they have had more exposure to the possible environmental toxin than did a group of controls similar to these people who did not develop the condition.
That kind of well-designed study discovered elevated rates of diabetes in people in the Native American population of Upstate New York who had elevated concentrations of PCBs in their blood stream compared to peers who did not. Another such study linked the concentrations of arsenic found in NHANES subject's urine to the likelihood those specific people would develop diabetes over time.
The next step in linking an environmental toxin to a disease is to find a mechanism that explains why the toxin might cause the specific disease. Researchers did that when they did rodent experiments proving that the pesticide Atrazine, whose use is most prevalent in the regions in the US that have the highest levels of obesity, caused insulin resistance and mitochondiral dysfunction.
(You can find links to the research cited above and others pointing to toxins in the environment causing genetic damage leading to diabetes HERE.)
With that in mind, lets look at what the researchers did in this new nitrates study. It turns out that all they did was compare "age adjusted increases in death rate from Alzheimer's, Parkinson's, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers" over the period from 1968 to 2005. Both grew.
As a control they compared the rise in nitrate use with the death rate from AIDS, Stroke, and Leukemia. These did not rise in tandem with increasing nitrate use.
QED? I don't think so. In fact, once again I am left wondering how someone trained in science could have considered this study worthy of publication.
For starters one gaping hole in the researchers logic is that they compared the death rate of one group of diseases which have no cure to the death rate of three diseases for which dramatic cure rates have occurred during the period from 1968 to 2005.
It takes about 25 seconds to realize that the death rate for AIDS, Stroke, and Leukemia have all plummeted since 1968 due to the advent of powerful and highly effective medications.
Leukemia was a death sentence in 1968 as anyone who ever wept their way through "Love Story" will remember.
AIDS was almost universally fatal when it first emerged in the early 1980s. Powerful drugs have turned it into a chronic condition.
The incidence of fatal stroke has decreased dramatically since the late 1960s due to the wide spread adoption of blood pressure screening and improvements in blood pressure medication.
Contrast the situation with the three conditions whose death rate the research would have you believe correlates with the rise in the use of nitrates. The researchers, rather surprisingly and, I would add, incorrectly, describe Alzheimers, Parkinsons, and Type 2 Diabetes thusly: "All of these diseases are associated with increased insulin resistance and DNA damage." What they neglect to mention is that not only are these three diseases still incurable, they have also undergone dramatic changes in how they are diagnosed, increases that mean many more people will have these conditions listed on their death certificates.
There is not a single drug for Alzheimers which delays its inevitable progression through deterioration to death. The drugs sold to the public with the claim they treat Alzheimers at best produce tiny "improvements" in functioning on specific cognitive tests which do not translate into changes observed in actual day to day function or behavior.
The researchers mention that the death rate from Alzheimers has skyrocketed over their period. But the explanation for this is two fold. First, improved health care means that people are living a lot longer--long enough to get Alzheimers which is relatively rare in people under the age of 80. Far fewer people made it into their mid-or late 80s in 1968. In addition, doctors did not diagnose "Alzheimers" in the 1960s for anything but unusual forms of dementia that occurred in relatively young people, aged 40-60. The use of the term "Alzheimers" for what used to be called "senile dementia" is relatively new.
Diabetes, as my readers know does have effective treatments. Unfortunately, they are not prescribed by the family doctors who treat patients. In fact, NHANES data found that the retreat from using insulin, which was more common in the 1960s to using heavily marketed oral drugs has led to a rise in the average A1c of the American diabetic over the 1990s, not a drop.
In addition, the diagnostic criteria for diagnosing Type 2 diabetes have undergone radical changes between 1968 and the present, to the point where comparing the death rate from diagnosed Type 2 in 1968 to the death rate from Diabetes diagnosed today is an apples-to-oranges situation. Most people who died from diabetes-related complications in the 1970s did so without ever getting a diabetes diagnosis.
So the fundamental methodology used in this study is deeply flawed. Beyond that, there is no attempt to go beyond vague hypothesis to explain the "correlation equals causation" conclusion here. Even if the correlation is real, which the study does not in any way prove, there are a lot of other things that have risen in tandem with the death rate from Type 2 diabetes: The number of bathrooms in the average house. The number of teams in Major League Baseball. The monthly premium for health insurance.
There are also some other far more scientifically valid environmental factors that have risen with the incidence of Type 2 diabetes--including the use of high fructose corn syrup in foods, the use of soy by products in foods, and the use of omega-6 vegetable oils in foods.
But to link anything in a causative way to a disease, you need to take that next step and find evidence that people who have the disease have more exposure to the supposed cause than other people otherwise similar to those people.
An elegant study recently showed much higher weight gain in a group of people drinking fructose-sweetened beverages to those drinking sugar sweetened beverages. You can read the details of that study HERE. This would take us a step closer to linking the invasion of our food supply by high fructose corn syrup to the advent of the obesity epidemic. Though because there are are so many different environmental correlations with the growth of both obesity and Type 2 diabetes, it is hard to assign the blame to any one.
But returning the the nitrate study, we see that its authors can point to no data showing that people who actually get Alzheimers or Type 2 diabetes consumed more nitrates than those who didn't. They don't show that people with high exposure to nitrates from fertilizer or industrial processes have more diabetes than people who did not have this exposure. No one has looked at the blood, urine, or tissues of people with Type 2 diabetes to see if they have higher levels of nitrosamines than people without the condition.
There is no proof that exposure to nitrates causes insulin resistance offered. And, for that matter, there isn't solid evidence showing a causative link between insulin resistance and Alzheimers and Type 2 Diabetes. Two thirds of the adult population is insulin resistant. Only about 10% ever develop diabetes.
The link is even more tenuous for Alzheimers. Fully one half of all people develop dementia if they live to be 80 or more including people who have normal insulin sensitivity. Since true Alzheimers can only be diagnosed on autopsy, many people whose cause of death is listed as "Alzheimers" actually have vascular dementia which is not clearly related to insulin resistance.
The scientific acceptance of this nitrate study--and the reason it got wide distribution in the media, is because the researchers linked nitrate exposure to eating processed foods and meat. In fact, among the factors they used to establish the rate of nitrate exposure was "annual sales at popular fast food chains, and sales for a major meat processing company."
So the religious belief: "meat is evil" and the sociological snob belief "people who eat fast food are fat slobs who cause their own diabetes" converge to give this woefully bad study credibility.
Mind you, it is possible that nitrates do cause diabetes, just as it is equally possible they don't. My point here is that this study doesn't begin to answer the question of whether there is such a relationship.
And its publication drops my respect for the people who peer review journal articles even further. They get paid huge amounts to provide their supposed scientific expertise. I do this for free. Yet over and over I am able to point out flaws in study design that should have been evident to anyone capable of logical thinking.
Something is wrong with this picture.
So you might expect when reports appeared all over the media recently, linking the increase in diabetes to nitrates in our food, I would have welcomed it as yet another factor pointing to an environmental cause for diabetes.
I might have, had I not read a detailed description of the research in question. Unfortunately, this study turns out to be yet another example of faith-based research--research that interprets correlations as causation. That is, researchers determine that two things happen at the same time and conclude one must have caused the other. As is often the case, this kind of conclusion is based not on hard scientific fact but on the fact that the correlation supports a a religious belief: "Meat and fast foods are evil."
Only the abstract of the study is available for free, here:
Epidemiological Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer's Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis . Journal of Alzheimer's Disease,Suzanne M. de la Monte et al., Volume 17, Number 3 / 2009. doi: 10.3233/JAD-2009-1070
But fortunately, a news report gives the salient details of this study. You can read it here:
Medical News Today: Researchers Find Possible Environmental Causes For Alzheimer's, Diabetes
To explain why this study is so flawed you need to know something about what has made other studies linking environmental substances to diabetes so compelling. In those studies, researchers take a group of people who developed diabetes and look for hard evidence that they have had more exposure to the possible environmental toxin than did a group of controls similar to these people who did not develop the condition.
That kind of well-designed study discovered elevated rates of diabetes in people in the Native American population of Upstate New York who had elevated concentrations of PCBs in their blood stream compared to peers who did not. Another such study linked the concentrations of arsenic found in NHANES subject's urine to the likelihood those specific people would develop diabetes over time.
The next step in linking an environmental toxin to a disease is to find a mechanism that explains why the toxin might cause the specific disease. Researchers did that when they did rodent experiments proving that the pesticide Atrazine, whose use is most prevalent in the regions in the US that have the highest levels of obesity, caused insulin resistance and mitochondiral dysfunction.
(You can find links to the research cited above and others pointing to toxins in the environment causing genetic damage leading to diabetes HERE.)
With that in mind, lets look at what the researchers did in this new nitrates study. It turns out that all they did was compare "age adjusted increases in death rate from Alzheimer's, Parkinson's, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers" over the period from 1968 to 2005. Both grew.
As a control they compared the rise in nitrate use with the death rate from AIDS, Stroke, and Leukemia. These did not rise in tandem with increasing nitrate use.
QED? I don't think so. In fact, once again I am left wondering how someone trained in science could have considered this study worthy of publication.
For starters one gaping hole in the researchers logic is that they compared the death rate of one group of diseases which have no cure to the death rate of three diseases for which dramatic cure rates have occurred during the period from 1968 to 2005.
It takes about 25 seconds to realize that the death rate for AIDS, Stroke, and Leukemia have all plummeted since 1968 due to the advent of powerful and highly effective medications.
Leukemia was a death sentence in 1968 as anyone who ever wept their way through "Love Story" will remember.
AIDS was almost universally fatal when it first emerged in the early 1980s. Powerful drugs have turned it into a chronic condition.
The incidence of fatal stroke has decreased dramatically since the late 1960s due to the wide spread adoption of blood pressure screening and improvements in blood pressure medication.
Contrast the situation with the three conditions whose death rate the research would have you believe correlates with the rise in the use of nitrates. The researchers, rather surprisingly and, I would add, incorrectly, describe Alzheimers, Parkinsons, and Type 2 Diabetes thusly: "All of these diseases are associated with increased insulin resistance and DNA damage." What they neglect to mention is that not only are these three diseases still incurable, they have also undergone dramatic changes in how they are diagnosed, increases that mean many more people will have these conditions listed on their death certificates.
There is not a single drug for Alzheimers which delays its inevitable progression through deterioration to death. The drugs sold to the public with the claim they treat Alzheimers at best produce tiny "improvements" in functioning on specific cognitive tests which do not translate into changes observed in actual day to day function or behavior.
The researchers mention that the death rate from Alzheimers has skyrocketed over their period. But the explanation for this is two fold. First, improved health care means that people are living a lot longer--long enough to get Alzheimers which is relatively rare in people under the age of 80. Far fewer people made it into their mid-or late 80s in 1968. In addition, doctors did not diagnose "Alzheimers" in the 1960s for anything but unusual forms of dementia that occurred in relatively young people, aged 40-60. The use of the term "Alzheimers" for what used to be called "senile dementia" is relatively new.
Diabetes, as my readers know does have effective treatments. Unfortunately, they are not prescribed by the family doctors who treat patients. In fact, NHANES data found that the retreat from using insulin, which was more common in the 1960s to using heavily marketed oral drugs has led to a rise in the average A1c of the American diabetic over the 1990s, not a drop.
In addition, the diagnostic criteria for diagnosing Type 2 diabetes have undergone radical changes between 1968 and the present, to the point where comparing the death rate from diagnosed Type 2 in 1968 to the death rate from Diabetes diagnosed today is an apples-to-oranges situation. Most people who died from diabetes-related complications in the 1970s did so without ever getting a diabetes diagnosis.
So the fundamental methodology used in this study is deeply flawed. Beyond that, there is no attempt to go beyond vague hypothesis to explain the "correlation equals causation" conclusion here. Even if the correlation is real, which the study does not in any way prove, there are a lot of other things that have risen in tandem with the death rate from Type 2 diabetes: The number of bathrooms in the average house. The number of teams in Major League Baseball. The monthly premium for health insurance.
There are also some other far more scientifically valid environmental factors that have risen with the incidence of Type 2 diabetes--including the use of high fructose corn syrup in foods, the use of soy by products in foods, and the use of omega-6 vegetable oils in foods.
But to link anything in a causative way to a disease, you need to take that next step and find evidence that people who have the disease have more exposure to the supposed cause than other people otherwise similar to those people.
An elegant study recently showed much higher weight gain in a group of people drinking fructose-sweetened beverages to those drinking sugar sweetened beverages. You can read the details of that study HERE. This would take us a step closer to linking the invasion of our food supply by high fructose corn syrup to the advent of the obesity epidemic. Though because there are are so many different environmental correlations with the growth of both obesity and Type 2 diabetes, it is hard to assign the blame to any one.
But returning the the nitrate study, we see that its authors can point to no data showing that people who actually get Alzheimers or Type 2 diabetes consumed more nitrates than those who didn't. They don't show that people with high exposure to nitrates from fertilizer or industrial processes have more diabetes than people who did not have this exposure. No one has looked at the blood, urine, or tissues of people with Type 2 diabetes to see if they have higher levels of nitrosamines than people without the condition.
There is no proof that exposure to nitrates causes insulin resistance offered. And, for that matter, there isn't solid evidence showing a causative link between insulin resistance and Alzheimers and Type 2 Diabetes. Two thirds of the adult population is insulin resistant. Only about 10% ever develop diabetes.
The link is even more tenuous for Alzheimers. Fully one half of all people develop dementia if they live to be 80 or more including people who have normal insulin sensitivity. Since true Alzheimers can only be diagnosed on autopsy, many people whose cause of death is listed as "Alzheimers" actually have vascular dementia which is not clearly related to insulin resistance.
The scientific acceptance of this nitrate study--and the reason it got wide distribution in the media, is because the researchers linked nitrate exposure to eating processed foods and meat. In fact, among the factors they used to establish the rate of nitrate exposure was "annual sales at popular fast food chains, and sales for a major meat processing company."
So the religious belief: "meat is evil" and the sociological snob belief "people who eat fast food are fat slobs who cause their own diabetes" converge to give this woefully bad study credibility.
Mind you, it is possible that nitrates do cause diabetes, just as it is equally possible they don't. My point here is that this study doesn't begin to answer the question of whether there is such a relationship.
And its publication drops my respect for the people who peer review journal articles even further. They get paid huge amounts to provide their supposed scientific expertise. I do this for free. Yet over and over I am able to point out flaws in study design that should have been evident to anyone capable of logical thinking.
Something is wrong with this picture.
July 13, 2009
Research Gives Insight into How to Measure Beta Cell Mass in Living People
Expensive diabetes drugs are being sold with the claim that they rejuvenate beta cells. Avandia, Actos, Januvia and Byetta are all promoted this way, and because they believe these claims doctors often insist their Type 2 patients stay on these costly drugs even when they aren't having any discernible effect on their blood sugar.
One reason the drug makers can make this claim is that it is difficult to disprove. That's because there is currently no way to measure the beta cell mass in a pancreas located inside a living person. Imaging fails because the size of the pancreas doesn't tell you anything about the density of beta cells. So researchers base their claim either on rodent studies--though rodents have very different blood sugar metabolisms than humans--or they estimate the beta cell mass of humans taking their drugs by measuring insulin or c-peptide levels and applying a formula, HOMA, to compute a number they believe represents the beta cell mass.
HOMA stands for "Homeostatic model assessment". The formula was created back in 1985 long before we had reliable measures of blood sugar variables or any way to measure beta cell mass. To learn the details of how HOMA is computed, read this essay:
Diabetes in Control: HOMA: Often Mentioned, Rarely Defined.
I have blogged before on how HOMA calculations fail to distinguish between insulin resistance and insulin deficiency and how this measure gave doctors the erroneous belief that Type 2s are largely insulin resistant, rather than, as turns out to be the case, insulin deficient.
I am particularly sensitive to this problem because when I plugged my numbers into the Oxford HOMA calculator some years ago, it told me I was seriously insulin resistant. It was only when I injected insulin that I discovered that I was very insulin sensitive--two or three units of fast acting insulin will cover 40-60 grams of carbohydrate for me, and I can hypo on 8 units of Lantus. So I felt vindicated when I learned that the HOMA formula labels many people "insulin resistant" who, in fact, are insulin deficient.
Now a new study takes another look at how the HOMA formula is used to estimate beta cell mass and finds it defective there, too. This is important because it is the HOMA calculation that is often used to support claims that various drugs are increasing beta cell mass.
The study is:
Functional Assessment of Pancreatic β-Cell Area in Humans. Juris J. Meier et al. Diabetes. July 2009, vol. 58, no. 7, 1595-1603. doi: 10.2337/db08-1611
The researchers here rounded up a group of unfortunate people who, because of serious medical problems, were about to have their pancreata removed. These subjects had a wide range of pancreatic function before surgery as they had different diseases some of which killed beta cells and some of which did not. The researchers gave them each a Glucose Tolerance Tests with C-peptide measurements before surgery.
After surgery their pancreases were carefully examined to find out exactly what their beta cell mass might be. This is not easily done because as soon as a pancreas is removed the enzymes it contains start to digest the pancreatic tissue. It is only over the past decade that techniques have been devised that allow researchers to examine beta cells shortly after death or after surgical excision of the pancreas.
What the researchers found was this:
With the exponential relationship that applies to the two hour glucose tolerance test result, if the two hour reading was up 3% your beta cell mass would be down 9% but if the 2 hour reading was up 6% your beta mass would be down 36%, if it was up 9% your beta mass might be down 81%. That gives you some idea of how much more intense an exponential relationship is compared to a linear relationship.
This suggests, too, why the glucose tolerance test and/or post-meal tests are so much more important than the fasting glucose test for diagnosing diabetes. Because small changes in the two hour test result point to larger changes in your beta cell mass.
What the researchers found in this study was that the blood test measure that best predicted the actual beta cell mass that they found when they examined the pancreas, was, "the C-peptide-to-glucose ratio determined 15 minutes after the glucose drink".
This is very interesting indeed, because until now we have been told because of earlier research that the 15-minute glucose tolerance test result was not predictive of anything and that only the 30 minute result was useful. That may be true if you look only at glucose levels, but this study makes it clear that it is not true if you include C-peptide levels.
Unfortunately, because of the belief that the 15 minutes result isn't useful, you will have to look long and hard to find other studies that measure 15 minutes C-peptide. Invariably when C-peptide is measured at all it is measured, fasting, at 1/2 hour intervals, and often only at the 2 hour mark.
The researchers also found that "a fasting C-peptide–to–glucose ratio already yielded a reasonably close correlation." It wasn't as good as the oral glucose tolerance test 15 minute measure, as shown by the "r" values. The lower the "r" value the better the correlation with an inverse result. The r value for the 15-minutes result was -.72 (-1.00 would have been perfect correlation and 0 would have been no correlation.). The r value for the fasting c-peptide/glucose ratio was -.63.
But here's the kicker. The researchers add "Homeostasis model assessment (HOMA) β-cell function was unrelated to β-cell area.
This is the same HOMA calculation drug company researchers are prone to use to support claims that their drugs are increasing beta cell mass.
I have long doubted that any oral drug can make a significant improvement in anyone's beta cell mass for several reasons. Long term studies show that over several years, after an initial improvement, the blood sugar control of people taking these drugs starts to declines. It does not improve the way it would if they had more beta cells cranking out insulin. This suggests that these drugs either stimulate insulin secretion--which is true of Januvia and Byetta--or make the same amount of insulin more effective, as is the case with Actos and Avandia.
But when you take people off all these drugs, within weeks their blood sugar control goes back to where it was before they started the drug, except in the case of the people for whom Byetta causes dramatic weight loss, who may have been blood sugars because they have 100 lbs less body weight and hence are more insulin sensitive.
Were a drug to actually regenerate beta cells, you'd expect to see blood sugar control increase over the long term and you'd also expect to see sustained better blood sugar control when the person stopped taking the drug. That neither of these effects occurs makes it very unlikely that these drugs are having this effect.
One cannot but wonder if perhaps there are similar studies to this one kept locked in drug company files, studies run to "prove" that Januvia or Byetta increased beta mass, whose publication was suppressed when the result was not found. The drug companies have been pushing this claim so hard for these drugs, that you would expect to see autopsy studies by now, years after the drug has been in use. And we know for a fact that drug companies have a long history of hiding or suppressing the publication of studies whose findings might lessen sales.
In any case, if you wonder about how your own beta cell mass is doing--and who doesn't--it would be nice to get that 15 minutes oral glucose tolerance test with C-peptide measurement that might give you a good read on this, but you won't. It isn't a standard lab test and doctors aren't likely to notice this particular research study since, because it doesn't promote a drug or confirm a strongly held belief, no one is going to bring it to their attention.
But what you can do is this: You can ask for a fasting C-peptide with glucose measurement every year, compute the C-peptide/glucose ratio, and track how it is progressing over time. This should give you some sense of how your beta mass is holding up.
If your doctor insists that you take Januvia or Byetta to "regrow your beta cells" insist on getting the fasting C-peptide test with fasting glucose measurement before you start the drug and then a year later. If you don't see improvement in the C-peptide/glucose ratio, you will know that the drug company claim is false. Then, if the drug hasn't made a significant improvement in your blood sugars, you'll know there is no reason for you--or your insurance company--to keep spending almost $200 a month on the drug.
Of course, if you have a personal history of cancer or a strong family history of cancer, you should not be taking Januvia, but that's another issue. Details here: Januvia and Cancer.
One reason the drug makers can make this claim is that it is difficult to disprove. That's because there is currently no way to measure the beta cell mass in a pancreas located inside a living person. Imaging fails because the size of the pancreas doesn't tell you anything about the density of beta cells. So researchers base their claim either on rodent studies--though rodents have very different blood sugar metabolisms than humans--or they estimate the beta cell mass of humans taking their drugs by measuring insulin or c-peptide levels and applying a formula, HOMA, to compute a number they believe represents the beta cell mass.
HOMA stands for "Homeostatic model assessment". The formula was created back in 1985 long before we had reliable measures of blood sugar variables or any way to measure beta cell mass. To learn the details of how HOMA is computed, read this essay:
Diabetes in Control: HOMA: Often Mentioned, Rarely Defined.
I have blogged before on how HOMA calculations fail to distinguish between insulin resistance and insulin deficiency and how this measure gave doctors the erroneous belief that Type 2s are largely insulin resistant, rather than, as turns out to be the case, insulin deficient.
I am particularly sensitive to this problem because when I plugged my numbers into the Oxford HOMA calculator some years ago, it told me I was seriously insulin resistant. It was only when I injected insulin that I discovered that I was very insulin sensitive--two or three units of fast acting insulin will cover 40-60 grams of carbohydrate for me, and I can hypo on 8 units of Lantus. So I felt vindicated when I learned that the HOMA formula labels many people "insulin resistant" who, in fact, are insulin deficient.
Now a new study takes another look at how the HOMA formula is used to estimate beta cell mass and finds it defective there, too. This is important because it is the HOMA calculation that is often used to support claims that various drugs are increasing beta cell mass.
The study is:
Functional Assessment of Pancreatic β-Cell Area in Humans. Juris J. Meier et al. Diabetes. July 2009, vol. 58, no. 7, 1595-1603. doi: 10.2337/db08-1611
The researchers here rounded up a group of unfortunate people who, because of serious medical problems, were about to have their pancreata removed. These subjects had a wide range of pancreatic function before surgery as they had different diseases some of which killed beta cells and some of which did not. The researchers gave them each a Glucose Tolerance Tests with C-peptide measurements before surgery.
After surgery their pancreases were carefully examined to find out exactly what their beta cell mass might be. This is not easily done because as soon as a pancreas is removed the enzymes it contains start to digest the pancreatic tissue. It is only over the past decade that techniques have been devised that allow researchers to examine beta cells shortly after death or after surgical excision of the pancreas.
What the researchers found was this:
β-Cell area was related to fasting glucose concentrations in an inverse linear fashion (r = −0.53, P = 0.0014) and to 120-min postchallenge glycemia in an inverse exponential fashion (r = −0.89)To give you a feeling for the difference between an "inverse linear" relationship and an "inverse exponential" relationship, let's look at a hypothetical example. In the linear relationship, if your fasting glucose was up, say, 3% then your beta cell mass would be down that same 3%. If the fasting glucose rose by 6%, your beta mass would go down 6%.
With the exponential relationship that applies to the two hour glucose tolerance test result, if the two hour reading was up 3% your beta cell mass would be down 9% but if the 2 hour reading was up 6% your beta mass would be down 36%, if it was up 9% your beta mass might be down 81%. That gives you some idea of how much more intense an exponential relationship is compared to a linear relationship.
This suggests, too, why the glucose tolerance test and/or post-meal tests are so much more important than the fasting glucose test for diagnosing diabetes. Because small changes in the two hour test result point to larger changes in your beta cell mass.
What the researchers found in this study was that the blood test measure that best predicted the actual beta cell mass that they found when they examined the pancreas, was, "the C-peptide-to-glucose ratio determined 15 minutes after the glucose drink".
This is very interesting indeed, because until now we have been told because of earlier research that the 15-minute glucose tolerance test result was not predictive of anything and that only the 30 minute result was useful. That may be true if you look only at glucose levels, but this study makes it clear that it is not true if you include C-peptide levels.
Unfortunately, because of the belief that the 15 minutes result isn't useful, you will have to look long and hard to find other studies that measure 15 minutes C-peptide. Invariably when C-peptide is measured at all it is measured, fasting, at 1/2 hour intervals, and often only at the 2 hour mark.
The researchers also found that "a fasting C-peptide–to–glucose ratio already yielded a reasonably close correlation." It wasn't as good as the oral glucose tolerance test 15 minute measure, as shown by the "r" values. The lower the "r" value the better the correlation with an inverse result. The r value for the 15-minutes result was -.72 (-1.00 would have been perfect correlation and 0 would have been no correlation.). The r value for the fasting c-peptide/glucose ratio was -.63.
But here's the kicker. The researchers add "Homeostasis model assessment (HOMA) β-cell function was unrelated to β-cell area.
This is the same HOMA calculation drug company researchers are prone to use to support claims that their drugs are increasing beta cell mass.
I have long doubted that any oral drug can make a significant improvement in anyone's beta cell mass for several reasons. Long term studies show that over several years, after an initial improvement, the blood sugar control of people taking these drugs starts to declines. It does not improve the way it would if they had more beta cells cranking out insulin. This suggests that these drugs either stimulate insulin secretion--which is true of Januvia and Byetta--or make the same amount of insulin more effective, as is the case with Actos and Avandia.
But when you take people off all these drugs, within weeks their blood sugar control goes back to where it was before they started the drug, except in the case of the people for whom Byetta causes dramatic weight loss, who may have been blood sugars because they have 100 lbs less body weight and hence are more insulin sensitive.
Were a drug to actually regenerate beta cells, you'd expect to see blood sugar control increase over the long term and you'd also expect to see sustained better blood sugar control when the person stopped taking the drug. That neither of these effects occurs makes it very unlikely that these drugs are having this effect.
One cannot but wonder if perhaps there are similar studies to this one kept locked in drug company files, studies run to "prove" that Januvia or Byetta increased beta mass, whose publication was suppressed when the result was not found. The drug companies have been pushing this claim so hard for these drugs, that you would expect to see autopsy studies by now, years after the drug has been in use. And we know for a fact that drug companies have a long history of hiding or suppressing the publication of studies whose findings might lessen sales.
In any case, if you wonder about how your own beta cell mass is doing--and who doesn't--it would be nice to get that 15 minutes oral glucose tolerance test with C-peptide measurement that might give you a good read on this, but you won't. It isn't a standard lab test and doctors aren't likely to notice this particular research study since, because it doesn't promote a drug or confirm a strongly held belief, no one is going to bring it to their attention.
But what you can do is this: You can ask for a fasting C-peptide with glucose measurement every year, compute the C-peptide/glucose ratio, and track how it is progressing over time. This should give you some sense of how your beta mass is holding up.
If your doctor insists that you take Januvia or Byetta to "regrow your beta cells" insist on getting the fasting C-peptide test with fasting glucose measurement before you start the drug and then a year later. If you don't see improvement in the C-peptide/glucose ratio, you will know that the drug company claim is false. Then, if the drug hasn't made a significant improvement in your blood sugars, you'll know there is no reason for you--or your insurance company--to keep spending almost $200 a month on the drug.
Of course, if you have a personal history of cancer or a strong family history of cancer, you should not be taking Januvia, but that's another issue. Details here: Januvia and Cancer.
July 8, 2009
Jenny's Real Life Gets Exciting!
Long time readers of my blog may remember that a few years ago I invited them to read a chapter of a Regency romance I'd posted in a contest. I didn't win that contest--though I made it to the top 20--but through my participation in that contest I made friends with another talented unpublished novelist who nagged me into working on my novels again and spent many months exchanging work and critiques with me. My friend's book sold a couple months ago, and she will be published in hardback next year.
And today I'm happy to announce that I, too, am, in the language used in the publishing trade press, officially a "debut novelist."
You can read the details of my book deal in this new blog I have set up:
The Adventure Begins: Avon Buys Lord Lighting
I will of course continue to keep up with the Diabetes news and update this blog and the Blood Sugar 101 web site. But I will be working full time on the second and third books I am now committed to deliver to my publisher. This deal gives me a foot in the door. If I can deliver, I have the chance of becoming a bestselling author. Avon is the top publisher of Romance and being acquired by them is like getting into the Top 24 in American Idol. I'll be competing with other new authors to build up a readership and I'll have to write fairly fast and very well to do this.
The latest word from my agent is that we are shooting for publication of the first book in November of 2010.
But what a thrill to be given a chance like this! And what a slap in the face for those who claim that the low carb diet decreases our mental abilities. I was low carbing at Bernstein levels when I wrote the first draft of this book and eating no more than 100 g a day when I did the many revisions it took to get published.
And today I'm happy to announce that I, too, am, in the language used in the publishing trade press, officially a "debut novelist."
You can read the details of my book deal in this new blog I have set up:
The Adventure Begins: Avon Buys Lord Lighting
I will of course continue to keep up with the Diabetes news and update this blog and the Blood Sugar 101 web site. But I will be working full time on the second and third books I am now committed to deliver to my publisher. This deal gives me a foot in the door. If I can deliver, I have the chance of becoming a bestselling author. Avon is the top publisher of Romance and being acquired by them is like getting into the Top 24 in American Idol. I'll be competing with other new authors to build up a readership and I'll have to write fairly fast and very well to do this.
The latest word from my agent is that we are shooting for publication of the first book in November of 2010.
But what a thrill to be given a chance like this! And what a slap in the face for those who claim that the low carb diet decreases our mental abilities. I was low carbing at Bernstein levels when I wrote the first draft of this book and eating no more than 100 g a day when I did the many revisions it took to get published.
July 6, 2009
The REAL Truth about Gastric Bypass's Supposed "Cure" of Type 2 Diabetes
You have probably heard a lot by now about how gastric bypass surgery can cure diabetes. Quite a few of my correspondents who are significantly overweight report being pressured by their doctors to sign up for weight loss surgery (WLS). Some family doctors are going so far as to refuse to prescribe less invasive treatments for high blood sugars in favor of insisting their patients have WLS.
Given this bias, it's worth looking closely at two new studies presented at the recent Annual Meeting of the American Society for Metabolic and Bariatric Surgery
First off, you need to understand that this convention is not an objective scientific gathering. It's the annual trade group meeting of the surgeons who profit--to the tune of $20,000 or more per surgery--from doing WLS.
The organization's membership is open to any licensed surgeon who has performed 25 weight loss surgeries. Associate membership is open to just about any medical professional willing to pay the membership fee. This group does not certify WLS surgeons. It does not even insist that the surgeons who join the organization prove that their patients survived the surgery or had good outcomes.
The mission of this WLS trade group is simple: to promote WLS and to provide "research" that will motivate insurers and Medicare to pay for ever more surgeries.
With that in mind, let's look at the studies presented at this latest conference because they are being reported in publications targeting endocrinologists and family doctors as showing that "Data confirms long-term effects of bariatric surgery on Type 2 diabetes."
I do not have access to the actual report, but there is a lengthy summary of it which appeared in the newsletter, Endocrine Today, which gives enough information to help us evaluate what the study really found.
The report begins by quoting a Dr. Christine Ren, identified only as an "associate professor of surgery at New York University School of Medicine," who says,
Dr. Ren's study gathered preoperative data on 95 patients (mean age, 49.3) who underwent laparoscopic adjustable gastric banding between 2002 and 2004. Five-year follow-up data were collected beginning in 2008.
She states, "At the five-year follow-up, mean BMI decreased from 46.3 to 35.0 — a mean value of 48.3% excess weight-loss."
As Dr. Ren explained it, “There was a sustained benefit — about 40% of patients had complete remission in their diabetes"
Complete remission sounds wonderful doesn't it? But what does "remission" really mean? Well, it turns out to mean this: "Mean fasting glucose decreased from 146 mg/dL preoperatively to 118.5 mg/dL at five years; mean HbA1c decreased from 7.53% to 6.58% (P<.001). "
I don't know about you, but I can get much better numbers than that without having my stomach permanently altered. I did it for seven years only by cutting way down on carbohydrates. Hundreds of my readers do this too.
But I would not consider a fasting blood sugar of 118.5 mg/dl (6.6 mmol/L) "complete remission." Nor would I consider an A1c of 6.58% nondiabetic.
And I'm not alone in this. The ultra-conservative ADA recently updated their position statements to define an A1c over 6.5% as diagnostic of diabetes.
The reason given by the ADA experts for choosing 6.5% as the diagnostic cutoff is that the incidence of retinopathy starts to rise significantly when A1c goes over 6.5%, though if you look at the data the ADA experts cite in their report, the incidence of retinopathy actually starts to rise when A1c goes over 6.0%. I urge all of you to read the ADA Position linking A1c to Diabetes diagnosis.
We all know that retinopathy is a relatively late diabetic complication. The ADA continues to use the presence of retinopathy as a diagnostic indicator for Diabetes, but since Retinopathy develops years after sudden onset diabetes (Type 1) that criterion makes as much sense as diagnosing AIDS by waiting until people develop brain lesions.
Other data suggest that heart disease incidence rises dramatically when A1c goes over 6.0% and that of neuropathy and kidney disease probably do too--as they begin to rise when post-meal blood sugars reach the pre-diabetic range.
Dr. Ren goes on to say,
A second study presented at the WLS trade show looked at long term outcomes of the even more dangerous Roux-en-Y gastric bypass surgery, where a large portion of the stomach is permanent amputated. Its findings also make it clear that the diabetes "cure" through WLS is completely illusory.
This study reports,
So let's get this straight. Amputating a large part of people's stomach resulted in a transient resolution" of diabetes, that did not last for almost half of them. Only 8% of those who were already diabetic enough to need insulin ended up better off than before they had the surgery.
How much more modest this data is than the results that were all over the media from other studies that claimed diabetes immediately went away in people who had WLS, "Like magic" and did not mention that this finding was based on blood sugar results a few weeks after surgery when the patients were not able to eat any carbs!
If we define "remissions" as dropping FBG or A1c just below Diagnostic Criteria for diabetes, a moderately low carb diet will achieve a higher rate of "remission" with the same or better long term statistics. And it will do so without risking the patients' life or condemning them to life-long nutritional problems.
What leaves me gasping with shock is this: the death rate of these surgeries runs quite high. You can read about the latest metastudy that came up with the statistics, HERE. Though the article was titled "Large Scale Analysis Finds Bariatric Surgery Relatively Safe," what was actually reported was a death rate of ".135% with 78 deaths reported among 57,918 patients."
No oral drug could ever be approved or sold to the public that killed 13 out of every thousand people who took it. But surgeries are not regulated. So surgeons have been performing WLS for decades even when they knew the death rate from this surgery was as high as 3 in every hundred.
Reading between the lines, this latest study was run in a cherry-picked fashion as in, "The data was accrued from participants in the ASMBS Bariatric Surgery Centers of Excellence program." The criteria for being a part of that program is undoubtedly a low mortality rate. So this statistic does not tell you what the death rate among average patients and doctors might be. The numbers I have seen elsewhere range from 1-3%.
Other studies have found the death rate from WLS much higher in some populations and found--more importantly--that it rises when the surgery is performed by doctors with little experience or skill. Since you have no way of knowing how skilled your surgeon may be, as doctors cover for each other and do not let word of their colleague's incompetence or drug addiction or alcoholism to become public, you have no way of knowing what your doctor's personal kill rate might be when you sign up for surgery.
But even those who do not die of the surgery--and some of those whose diabetes "goes into remission" are at high risk of serious nutrition deficiencies after WLS. This is because altering the stomach often destroys the ability to absorb important minerals. This nutritional deficiency syndrome is so severe that a 2009 Mayo Clinic study found that people who have had WLS have twice the risk of fractures as the normal population. A review published in 2017 updated this finding with citations of many more studies confirming the serious impacts of nutritional deficiencies caused by weight loss surgeries.
Many people who have had the surgery must go to the hospital periodically for intravenous mineral supplementation without which they can die.
IF your doctor suggests that WLS is a quick way to eliminate your diabetes, remember that he learned this "Fact" from the studies that looked at blood sugar a few weeks or months after the surgery when the stomach is so tiny people cannot eat enough carbohydrates to see elevated blood sugars.
Remember too that the studies show that people with diabetes who need insulin probably won't see an improvement, because if your beta cells are dead, the surgery is not going to be able to fix them.
All WLS does to "reverse diabetes" is make significant carb restriction non-negotiable. Eat enough carbs to raise your blood sugar, early on after the surgery, and you'll vomit it all back up. There isn't room in your tiny stomach pouch for enough food to raise your blood sugar.
Over time the pouch stretches and your blood sugar will go right back up as you eat more food. You didn't reverse anything. You simply lowered your blood sugar by making it impossible to eat carbs.
You can cut way back on carbs without surgery. Metformin can cut way down on hunger and when combined with a carb restricted diet can also give you blood sugars at least as good as what these surgeries produce, and possibly better.
But don't expect to hear this from the media. The WLS surgeons have unleashed a formidable PR machine. They make their claims on TV unchallenged. They promote their surgeries with highly questionable research conducted by doctors who profit personally from the growth of the WLS patient base.
Given this bias, it's worth looking closely at two new studies presented at the recent Annual Meeting of the American Society for Metabolic and Bariatric Surgery
First off, you need to understand that this convention is not an objective scientific gathering. It's the annual trade group meeting of the surgeons who profit--to the tune of $20,000 or more per surgery--from doing WLS.
The organization's membership is open to any licensed surgeon who has performed 25 weight loss surgeries. Associate membership is open to just about any medical professional willing to pay the membership fee. This group does not certify WLS surgeons. It does not even insist that the surgeons who join the organization prove that their patients survived the surgery or had good outcomes.
The mission of this WLS trade group is simple: to promote WLS and to provide "research" that will motivate insurers and Medicare to pay for ever more surgeries.
With that in mind, let's look at the studies presented at this latest conference because they are being reported in publications targeting endocrinologists and family doctors as showing that "Data confirms long-term effects of bariatric surgery on Type 2 diabetes."
I do not have access to the actual report, but there is a lengthy summary of it which appeared in the newsletter, Endocrine Today, which gives enough information to help us evaluate what the study really found.
The report begins by quoting a Dr. Christine Ren, identified only as an "associate professor of surgery at New York University School of Medicine," who says,
“This is a strong message to physicians and endocrinologists that gastric banding should be very seriously considered in the morbidly obese diabetic population because it offers the best chance to have better control or remission of their diabetes long-term [emphasis mine].Unmentioned in the report is the fact that Dr. Ren advertises herself publicly, on a web site that at the time had the URL"thinforlife.med.nyu.edu" as "the Leading Surgeon for lap band surgery in the U.S." So she is hardly an objective source of endocrinological advice.
Dr. Ren's study gathered preoperative data on 95 patients (mean age, 49.3) who underwent laparoscopic adjustable gastric banding between 2002 and 2004. Five-year follow-up data were collected beginning in 2008.
She states, "At the five-year follow-up, mean BMI decreased from 46.3 to 35.0 — a mean value of 48.3% excess weight-loss."
As Dr. Ren explained it, “There was a sustained benefit — about 40% of patients had complete remission in their diabetes"
Complete remission sounds wonderful doesn't it? But what does "remission" really mean? Well, it turns out to mean this: "Mean fasting glucose decreased from 146 mg/dL preoperatively to 118.5 mg/dL at five years; mean HbA1c decreased from 7.53% to 6.58% (P<.001). "
I don't know about you, but I can get much better numbers than that without having my stomach permanently altered. I did it for seven years only by cutting way down on carbohydrates. Hundreds of my readers do this too.
But I would not consider a fasting blood sugar of 118.5 mg/dl (6.6 mmol/L) "complete remission." Nor would I consider an A1c of 6.58% nondiabetic.
And I'm not alone in this. The ultra-conservative ADA recently updated their position statements to define an A1c over 6.5% as diagnostic of diabetes.
The reason given by the ADA experts for choosing 6.5% as the diagnostic cutoff is that the incidence of retinopathy starts to rise significantly when A1c goes over 6.5%, though if you look at the data the ADA experts cite in their report, the incidence of retinopathy actually starts to rise when A1c goes over 6.0%. I urge all of you to read the ADA Position linking A1c to Diabetes diagnosis.
We all know that retinopathy is a relatively late diabetic complication. The ADA continues to use the presence of retinopathy as a diagnostic indicator for Diabetes, but since Retinopathy develops years after sudden onset diabetes (Type 1) that criterion makes as much sense as diagnosing AIDS by waiting until people develop brain lesions.
Other data suggest that heart disease incidence rises dramatically when A1c goes over 6.0% and that of neuropathy and kidney disease probably do too--as they begin to rise when post-meal blood sugars reach the pre-diabetic range.
Dr. Ren goes on to say,
"about 40% of patients had complete remission in their diabetes. This was confirmed with normal fasting blood sugar, normal HbA1c and they were completely off all medications including insulin,” Ren said. “In addition, there were another 40% of patients who had improvements in diabetes as shown by a decrease in their medication, improvements in fasting blood glucose control and improvements in HbA1c.” Diabetes was resolved in 43% of patients, for a total improvement/resolution rate of 83%.If we define "complete remission" of diabetes as achieving A1c under 7% and FBG under 125 mg/dl, my guess is that a lot more than 43% of us have "resolved" our diabetes with much less invasive approaches. Even if we define a diabetes cure as meaning we achieve truly "normal" blood sugars--i.e. FBG under 100 mg/dl and post-meal numbers under 140 mg/dl at two hours after eating, most of my long term readers may be surprised to discover they have long been are "cured" of their diabetes.
A second study presented at the WLS trade show looked at long term outcomes of the even more dangerous Roux-en-Y gastric bypass surgery, where a large portion of the stomach is permanent amputated. Its findings also make it clear that the diabetes "cure" through WLS is completely illusory.
This study reports,
Complete resolution was achieved in 157 patients who also had a decrease in mean BMI from 50.2 before surgery to 31.3 after surgery. Forty-three percent of these patients subsequently had type 2 diabetes recurrence and associated weight gain [emphasis mine].The chief researcher in this study is quoted as saying, "“When looking at the insulin-controlled diabetic patients, 80% had resolution at some point, but recurred in 72%."
So let's get this straight. Amputating a large part of people's stomach resulted in a transient resolution" of diabetes, that did not last for almost half of them. Only 8% of those who were already diabetic enough to need insulin ended up better off than before they had the surgery.
How much more modest this data is than the results that were all over the media from other studies that claimed diabetes immediately went away in people who had WLS, "Like magic" and did not mention that this finding was based on blood sugar results a few weeks after surgery when the patients were not able to eat any carbs!
If we define "remissions" as dropping FBG or A1c just below Diagnostic Criteria for diabetes, a moderately low carb diet will achieve a higher rate of "remission" with the same or better long term statistics. And it will do so without risking the patients' life or condemning them to life-long nutritional problems.
What leaves me gasping with shock is this: the death rate of these surgeries runs quite high. You can read about the latest metastudy that came up with the statistics, HERE. Though the article was titled "Large Scale Analysis Finds Bariatric Surgery Relatively Safe," what was actually reported was a death rate of ".135% with 78 deaths reported among 57,918 patients."
No oral drug could ever be approved or sold to the public that killed 13 out of every thousand people who took it. But surgeries are not regulated. So surgeons have been performing WLS for decades even when they knew the death rate from this surgery was as high as 3 in every hundred.
Reading between the lines, this latest study was run in a cherry-picked fashion as in, "The data was accrued from participants in the ASMBS Bariatric Surgery Centers of Excellence program." The criteria for being a part of that program is undoubtedly a low mortality rate. So this statistic does not tell you what the death rate among average patients and doctors might be. The numbers I have seen elsewhere range from 1-3%.
Other studies have found the death rate from WLS much higher in some populations and found--more importantly--that it rises when the surgery is performed by doctors with little experience or skill. Since you have no way of knowing how skilled your surgeon may be, as doctors cover for each other and do not let word of their colleague's incompetence or drug addiction or alcoholism to become public, you have no way of knowing what your doctor's personal kill rate might be when you sign up for surgery.
But even those who do not die of the surgery--and some of those whose diabetes "goes into remission" are at high risk of serious nutrition deficiencies after WLS. This is because altering the stomach often destroys the ability to absorb important minerals. This nutritional deficiency syndrome is so severe that a 2009 Mayo Clinic study found that people who have had WLS have twice the risk of fractures as the normal population. A review published in 2017 updated this finding with citations of many more studies confirming the serious impacts of nutritional deficiencies caused by weight loss surgeries.
Many people who have had the surgery must go to the hospital periodically for intravenous mineral supplementation without which they can die.
IF your doctor suggests that WLS is a quick way to eliminate your diabetes, remember that he learned this "Fact" from the studies that looked at blood sugar a few weeks or months after the surgery when the stomach is so tiny people cannot eat enough carbohydrates to see elevated blood sugars.
Remember too that the studies show that people with diabetes who need insulin probably won't see an improvement, because if your beta cells are dead, the surgery is not going to be able to fix them.
All WLS does to "reverse diabetes" is make significant carb restriction non-negotiable. Eat enough carbs to raise your blood sugar, early on after the surgery, and you'll vomit it all back up. There isn't room in your tiny stomach pouch for enough food to raise your blood sugar.
Over time the pouch stretches and your blood sugar will go right back up as you eat more food. You didn't reverse anything. You simply lowered your blood sugar by making it impossible to eat carbs.
You can cut way back on carbs without surgery. Metformin can cut way down on hunger and when combined with a carb restricted diet can also give you blood sugars at least as good as what these surgeries produce, and possibly better.
But don't expect to hear this from the media. The WLS surgeons have unleashed a formidable PR machine. They make their claims on TV unchallenged. They promote their surgeries with highly questionable research conducted by doctors who profit personally from the growth of the WLS patient base.
July 1, 2009
ACCORD Redux: Low A1c Does Not Raise Risk of Death
Not a week goes by that I don't get at least one email from a reader whose doctor has warned them that it would be dangerous to lower their A1c to 6.5%.
I have blogged several times about why ignorant doctors are dispensing this dangerous advice. You can read past discussions HERE, HERE, and HERE.
ACCORD was the large study that supposedly found the correlation between lowering A1c and increased risk of heart attack. A very similar study, ADVANCE, found no such correlation, which given all we know about the impact of elevated blood sugars on heart health should have made doctors question the findings of ADVANCE more closely. But few seem to have done this.
Fortunately, a few have. Diabetes in Control recently reported on a presentation given at the recent ADA Scientific Sessions which found that further analysis of ACCORD data "did not confirm the proposed theory that low A1c levels might be the cause" of the elevated risk of death in the ACCORD patients who attempted to achieve tighter control.
Matthew C. Riddle, MD, Professor of Medicine, Oregon Health Science University and a member of the Glycemia Management Group of ACCORD, who was a site principal investigator for the ACCORD study is quoted as saying,
I urge you to read the whole Diabetes in Control report. You'll find it here:
ADA - Low Glucose Levels Do Not Explain Excess Deaths in ACCORD Trial:A1c of less than 7% is not a predictor of mortality risk in Type 2 diabetes and the converse is true in that higher A1cs do increase the risk of mortality. For every 1% higher A1c level above 6%, the risk of death increases by 20%.
If your doctor is telling you that lowering your A1c is dangerous, print out this article for him or her.
Then find a new doctor. There is a huge amount of evidence proving that lowering A1c below 7.0% lowers the risk of kidney failure, blindness, and yes, heart attack.
Here's a recent metastudy published in May that confirms that "Intensive glycaemic control resulted in a 17% reduction in events of non-fatal myocardial infarction [i.e. heart attack], and a 15% reduction in events of coronary heart disease."
This study found that intensive control also has " no significant effect on events of stroke or all-cause mortality." While that might sound like bad news about tight control, since you'd hope it would improve lifespan, in fact, it is good news. It means that tight control does NOT raise the risk of death, contrary to the erroneous conclusion so many doctors are drawing from ACCORD.
Here is a link to that metastudy:
Effect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: a meta-analysis of randomised controlled trials Kausik K Ray et al. The Lancet, Volume 373, Issue 9677, Pages 1765 - 1772, 23 May 2009 doi:10.1016/S0140-6736(09)60697-8
Personally, given the choice between dying of a heart attack at age 85 blind, on dialysis, and with my leg amputated, or dying of a heart attack at age 85 with normal vision, kidneys, and nerves, I know which choice I'd make--and to achieve that choice I will need to aggressively pursue normal blood sugars.
The only time that lowering A1c has not been shown to be effective in reducing diabetes-related mortality in a group as a whole is when the studies involve large groups of elderly victims of medical incompetence who have spent at least ten years with A1cs in the 10% range or higher. These are people whose organs have already been ravaged by uncontrolled high blood sugars, often to where irreversible damage has occurred. Researchers then load them up with a cocktail of drugs several of which, Avandia and Actos, are known to cause heart failure. And a very small rise in the incidence of death occurs.
Getting back to the Diabetes in Control report, note that once again when reporting mortality in ACCORD researchers resorted to using the magnifying statistical technique called "Risk." Pause for a moment and consider what statistical risk measures. If I have two groups of a thousand people, and one group experiences 2 deaths of a certain type while the other experiences 3 deaths, the risk of death in the second group is 50% higher, because the number 3 is 1 more, i.e. 50% higher than 2. But the actual difference in the incidence of death in each group is tiny and possibly not even statistically significant.
In ACCORD the increased incidence of death in the tight control group was slight--the actual number of excess deaths. It only looked scary because it was reported as a 20% higher risk. Chances are that your doctor who may have taken one statistics class 25 years ago is not even aware of the difference between the two statistical measures or how they inflate findings. Statins are also promoted heavily using "risk" amplified statistics rather than incidence statistics because citing "risk" puffs up results that otherwise are unimpressive.
In fact, one very interesting finding of several recent studies of diabetes and heart attack is that researchers report that they are seeing far fewer heart attack deaths in their study population of Diabetics than they expected. So much lower, in fact, that important studies like JPAD, a study that attempted to investigate the impact of taking aspirin on cardiovascular deaths among people with diabetes are being described as "statistically underpowered due to an unexpectedly low rate of clinical events." (Medscape report on JPAD).
This low incidence of heart attacks in a population that used to have a lot more of them may be the result of much better blood pressure control over recent decades or even, dare we say, of better blood sugar control as a result of the classic 1990s studies DCCT and UKPDS which proved that lowering A1c decreased complications.
There is nothing found in analysis of data from ACCORD or any other study that suggests anything but this: further lowering of blood sugar, over time, is likely to result in further lowering of heart attack incidence and better long term, complication-free survival.
All this suggests that there is one more risk factor that will impact your health as you grow older with diabetes: The competence of your doctor. The better your doctor understands how elevated blood sugars cause complications, the better will be the care you receive. A doctor who does not understand why normal blood sugars will produce normal health is as dangerous to your health as one who puts you on a diet of daily banana splits.
I have blogged several times about why ignorant doctors are dispensing this dangerous advice. You can read past discussions HERE, HERE, and HERE.
ACCORD was the large study that supposedly found the correlation between lowering A1c and increased risk of heart attack. A very similar study, ADVANCE, found no such correlation, which given all we know about the impact of elevated blood sugars on heart health should have made doctors question the findings of ADVANCE more closely. But few seem to have done this.
Fortunately, a few have. Diabetes in Control recently reported on a presentation given at the recent ADA Scientific Sessions which found that further analysis of ACCORD data "did not confirm the proposed theory that low A1c levels might be the cause" of the elevated risk of death in the ACCORD patients who attempted to achieve tighter control.
Matthew C. Riddle, MD, Professor of Medicine, Oregon Health Science University and a member of the Glycemia Management Group of ACCORD, who was a site principal investigator for the ACCORD study is quoted as saying,
An A1c below 7% alone does not appear to explain the excess deaths in the ACCORD trial and is not necessarily a predictor of mortality risk...Further, the rate of one-year change in A1c showed that a greater decline in A1c was associated with a lower risk of death.Translated into English this means that, as we all knew before this outlier study was published, lowering A1c below 7.0% improves your chance of living longer. It does not impede it.
I urge you to read the whole Diabetes in Control report. You'll find it here:
ADA - Low Glucose Levels Do Not Explain Excess Deaths in ACCORD Trial:A1c of less than 7% is not a predictor of mortality risk in Type 2 diabetes and the converse is true in that higher A1cs do increase the risk of mortality. For every 1% higher A1c level above 6%, the risk of death increases by 20%.
If your doctor is telling you that lowering your A1c is dangerous, print out this article for him or her.
Then find a new doctor. There is a huge amount of evidence proving that lowering A1c below 7.0% lowers the risk of kidney failure, blindness, and yes, heart attack.
Here's a recent metastudy published in May that confirms that "Intensive glycaemic control resulted in a 17% reduction in events of non-fatal myocardial infarction [i.e. heart attack], and a 15% reduction in events of coronary heart disease."
This study found that intensive control also has " no significant effect on events of stroke or all-cause mortality." While that might sound like bad news about tight control, since you'd hope it would improve lifespan, in fact, it is good news. It means that tight control does NOT raise the risk of death, contrary to the erroneous conclusion so many doctors are drawing from ACCORD.
Here is a link to that metastudy:
Effect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: a meta-analysis of randomised controlled trials Kausik K Ray et al. The Lancet, Volume 373, Issue 9677, Pages 1765 - 1772, 23 May 2009 doi:10.1016/S0140-6736(09)60697-8
Personally, given the choice between dying of a heart attack at age 85 blind, on dialysis, and with my leg amputated, or dying of a heart attack at age 85 with normal vision, kidneys, and nerves, I know which choice I'd make--and to achieve that choice I will need to aggressively pursue normal blood sugars.
The only time that lowering A1c has not been shown to be effective in reducing diabetes-related mortality in a group as a whole is when the studies involve large groups of elderly victims of medical incompetence who have spent at least ten years with A1cs in the 10% range or higher. These are people whose organs have already been ravaged by uncontrolled high blood sugars, often to where irreversible damage has occurred. Researchers then load them up with a cocktail of drugs several of which, Avandia and Actos, are known to cause heart failure. And a very small rise in the incidence of death occurs.
Getting back to the Diabetes in Control report, note that once again when reporting mortality in ACCORD researchers resorted to using the magnifying statistical technique called "Risk." Pause for a moment and consider what statistical risk measures. If I have two groups of a thousand people, and one group experiences 2 deaths of a certain type while the other experiences 3 deaths, the risk of death in the second group is 50% higher, because the number 3 is 1 more, i.e. 50% higher than 2. But the actual difference in the incidence of death in each group is tiny and possibly not even statistically significant.
In ACCORD the increased incidence of death in the tight control group was slight--the actual number of excess deaths. It only looked scary because it was reported as a 20% higher risk. Chances are that your doctor who may have taken one statistics class 25 years ago is not even aware of the difference between the two statistical measures or how they inflate findings. Statins are also promoted heavily using "risk" amplified statistics rather than incidence statistics because citing "risk" puffs up results that otherwise are unimpressive.
In fact, one very interesting finding of several recent studies of diabetes and heart attack is that researchers report that they are seeing far fewer heart attack deaths in their study population of Diabetics than they expected. So much lower, in fact, that important studies like JPAD, a study that attempted to investigate the impact of taking aspirin on cardiovascular deaths among people with diabetes are being described as "statistically underpowered due to an unexpectedly low rate of clinical events." (Medscape report on JPAD).
This low incidence of heart attacks in a population that used to have a lot more of them may be the result of much better blood pressure control over recent decades or even, dare we say, of better blood sugar control as a result of the classic 1990s studies DCCT and UKPDS which proved that lowering A1c decreased complications.
There is nothing found in analysis of data from ACCORD or any other study that suggests anything but this: further lowering of blood sugar, over time, is likely to result in further lowering of heart attack incidence and better long term, complication-free survival.
All this suggests that there is one more risk factor that will impact your health as you grow older with diabetes: The competence of your doctor. The better your doctor understands how elevated blood sugars cause complications, the better will be the care you receive. A doctor who does not understand why normal blood sugars will produce normal health is as dangerous to your health as one who puts you on a diet of daily banana splits.
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