I've received several worried emails over the past week written in response to a study which is being highlighted by the vegan/low fat/low-carb-diet-haters, who are using it to supposedly prove that eating a low carb diet rich in meat will acidify your blood and give you diabetes.
This article is summarized here:
http://www.medindia.net/news/higher-dietary-acid-load-increases-diabetes-risk-127666-1.htm
Dr. Weil, who has earned millions promoting his own brand of faddish health advice summarizes it here: http://www.drweil.com/drw/u/WBL02378/Surprise-Diabetes-Threat.html
I went and read the actual study, which you can find in its full form here:
Dietary acid load and risk of type 2 diabetes: the E3N-EPICcohort study
Here's my take on it:
I am always very suspicious of the findings of any large study that draws its conclusions from questionnaires purporting to measure what people are supposed to have eaten over a set period of time. And it turns out that this is exactly what was done here.
The measures of blood acidity used in this study, PRAL and NEAP, are not determined by measuring blood acid in the participants. Instead, they are computed using a formula which was applied to the answers given in response to a standardized dietary questionnaires filled in by study participants. You can read a critique of the methodology used to establish the forumulas used to convert these questionnaire responses to estimated blood acidity here: Critique on equations of net endogenous acid production (NEAP) and indirect proof of constant organic acid excretion
But even if this study is wrong that the formulas are flawed, since the level of blood acids are not actually measured, the reliability of the study result all comes down to the quality of the questionnaires used. And that is something I have personal experience with, as I was a subject years ago in a study of low carb dieters, a study that used one of these standardized nutritional survey questionnaires.
As the study proceeded I filled out this multiple-choice questionnaire several times. At one point, the nutritionist running the study mailed me my personal dietary analysis based on the answers I had given. Since this occurred during the year when, to lose weight successfully, I had taken to actively logging every bite I ate using LifeForm software, and carefully measuring portion sizes, too, I was able to compare my actual intake, as tracked in my log with what the questionnaire said I had eaten.
The questionnaire's results weren't even close. It ascribed to me a much higher calorie intake than what I was actually eating, and even more significantly, came up with a completely different breakdown of carbs, protein, and fat--one that gave me a much higher carb intake than what I was actually eating. One that would have completely knocked me out of the ketogenic state that random tests with ketone strips confirmed I was maintaining.
The total failure of the questionnaire to reflect my dietary intake didn't surprise me, though, because the multiple choice questions that made up the questionnaire were written in such a way that it was impossible for me to give accurate answers. For example, there was no option to answer "never" to many of the questions about my intake of high carb foods like potatoes. Instead I had a choice of reporting I had eaten potatoes "1 to 5" times in the previous month.
And though the questionnaire might ask about how often I had eaten red meat, or even about how often I had eaten "hamburger" it did not ask any questions that would make it possible to determine whether the "meat" I reported eating was the pink slime laced with MSG eaten at McDonalds or a home cooked burger made of high quality ground sirloin.
Even worse, there was no way that the questions posed by the questionnaire could determine if the "red meat" I had eaten had been accompanied by a big white bread bun and a big serving of fries. A person eating a stack of pancakes with syrup, eggs, and ham for breakfast who fills in this questionnaires is scored as eating "meat", in these questionnaires, though any future sorry metabolic outcome linked to eating this kind breakfast more likely to be due to its high carb intake, the high fructose in the syrup and the phosphates and other chemicals in the ham.
So these fatally flawed questionnaires will point the finger at "meat" when the real nutritional culprits may be something else entirely.
That's why I would not don't take this study too seriously. If you had a study where blood acid levels were actually measured in a large population over a long period of time and the measured high blood acids were found to be correlated with a nasty health outcome, it would be worth thinking about, but the costs of that kind of study are prohibitive, so it isn't likely to happen. But as we have no way of even knowing if the participants in this study really had high levels of acid in their blood, and if the higher level of diabetes found in people who said they ate a lot of meat was caused by the meat or what they ate alongside of the meat, the rest of the study's conclusions are really a stretch.
That said, as I have written before, people eating low carb diets should be careful to eat quality, unprocessed meats and, as discussed in an earlier blog post, it is very wise to avoid eating meats laced with the inorganic phosphates that will damage your kidneys and heart. A low carb diet whose protein component is made up largely of fast food burger patties, processed foods, and supermarket bacon is not a healthy diet.
If you are going to eat a lot of meat (which many of us who eat low carb diets do not do) it is a good idea to eat organic meats if you are going to be eating a lot of meat fat, because pesticides and other environmental toxins do tend to be deposited in animal fat.
Also,because the fatty acid composition of the fat of the animals we eat reflect the fats they eat, the fat from animals fattened on the currently fashionable "vegetarian" animal feeds made up of corn and corn oil may contain higher levels of inflammation-producing omega-6 fatty acids than meat did in the past. So it may no longer be a good idea to eat the fat found in supermarket meats. if you can find meat from pastured animals, that would be a better choice. I am coming to think it might be healthier to get the fat component in your diet from butters made from pastured cows and from non-processed imported cheeses rather than from consuming big chunks of animal fat.
November 21, 2013
November 14, 2013
Study: Lower Your Cholesterol and Raise Your Risk of Death Following Mainstream Diet Advice
You've been hearing for decades about how a healthy diet is one that lowers your intake of saturated fats and replaces them with "healthy" unsaturated oils. This, you have been told, will lower your cholesterol and your risk of having a heart attack.
What you probably didn't hear is that a study published in the British Medical Journal (BMJ) February of this past year found that though the first claim is true--swapping out saturated fats for vegetable oils will lower your cholesterol--if the oil you use instead of saturated fat is full of omega-6 fatty acid, like safflower oil or corn oil, the second claim is completely false.
The study found that when men who had already had a heart attack replaced saturated fats with safflower oil and ate margarine made with safflower oil they significantly raised the risk that they would die of a heart attack, stroke or, in fact, any cause of death, over the next five years.
How significantly was that risk raised? The study states: "Among the control and intervention groups combined, an increase of 5% of food energy from unspecified PUFA [polyunsaturated fatty acids] predicted about 30% higher risk of cardiovascular death and all cause mortality.
A reduction in SFA [saturated fat] and increase in the PUFA:SFA ratio were also associated with increased risks of all cause and cardiovascular mortality." In short, the more they replaced saturated fat with "healthy" polyunsaturated oil the more likely they were to die.
I was only made aware of this study last week, when the Canadian Medical Association Journal (CMAJ) published an opinion piece questioning whether the government should be putting "heart healthy" labels on corn oil and other polyunsaturated fats. (Details HERE.) They cited the February BMJ study in their write-up.
What doesn't come across in the small amount of press the CMAJ article got is something that makes the BMJ study even more significant: The data that this finding was based on was 40 years old. It was collected during the Sydney Diet Heart Study, a randomized controlled trial conducted in 1966-73.
This was one of the many landmark interventional studies whose result was used to convince doctors that replacing saturated fats with polyunsaturated fats would lower cholesterol and, by implication, prevent heart disease.
But while the authors of the original study published the finding that the polyunsaturated fats would lower both cholesterol and triglycerides, they did not look to see whether lowering cholesterol with this intervention actually helped prevent heart-related deaths.
They eventually admitted in a study published in 1978--a full 5 years after they began to publish their results--that there was a higher "all cause mortality" in the group eating the safflower oil, but they did not look at whether these deaths were from cardiovascular-related causes. This was a surprising omission, given the point of the dietary intervention--to lower cholesterol in order to prevent heart attacks.
So it was only in the last few years that a new group of researchers were able to go back to the original study's raw data and take another look at it. When they did so, they discovered what they term "previously missing data." This "missing data" was the data that led to the conclusion that there was a 30% greater risk of cardiovascular death among the people in the study who ate the cholesterol-lowering oil.
Getting at this missing data was not a trivial process. The original study data had been stored on 9-track tape--the kind you can see at left--which used to be used by IBM 360 series mainframe computers. There are only a very few data recovery specialists around who can still read these kinds of tapes.
Once they recovered the data, the researchers did a very careful analysis, teasing out other factors that might have affected the death rate and, most significantly, analyzing whether the transfat associated with the margarine the test subjects ate might have explained the higher death rate. They conclude it did not.
They also point out that this re-analysis of the data echoes what was found in two other re-analyses of 1960-70s era cholesterol/heart diet trials: Linoleic acid, with its high proportion of Omega-6 fatty acid and complete lack of Omega-3 fatty acid is really toxic stuff.
You can read the whole BMJ study here:
Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.
Omega-6 Fatty Acids Promote Inflammation
The researchers believe that the reason that the polyunsaturated oils used in these cholesterol-lowering diets were so toxic was because the vegetable oils used were very high in Linoleic Acid, an Omega-6 fatty acid, and devoid of the countervailing Omega-3 fatty acids you need to consume to keep Omega-6 fatty acids from promoting inflammation.
So, okay. Safflower oil is now out of your diet. But it turns out that safflower oil is not the only common vegetable oil that is rich in linoleic oil. Corn oil is very high in it, too. You can see a complete list of oils sorted by their percentage of Linoleic acid HERE.
Finally, though health nuts who still fear that eating saturated fat will kill them will tell you that canola oil and flaxseed oil are healthier alternatives, neither of these oils has been a part of the human diet for any significant period of time the way animal and dairy fats have been.
Canola oil does contain Omega-3 fatty acids, but the process used to take away its rank smell and keep it from going rancid is likely to damage them. Damaged Omega-3 oils is not healthy. Flaxseed oil is the recently renamed stuff we used to call linseed oil and use for mixing up oil based paint--which it often tastes like. It's safe to eat if you keep it refrigerated and don't let it go rancid, but since it is not a traditional food, I would suggest eating it in small quantities.
Palm oil is another fat that has recently made its way into our food system, as manufacturers are using it as a replacement for the hydrogenated oils full of transfat. But while there may be health benefits from consuming the palm oil eaten in traditional societies, the industrially processed palm oil that is appearing on supermarket shelves is very different stuff and may very well be harboring transfat-like molecules that escape the FDA labeling requirements. And besides that, it often tastes--and refuses to melt--suspiciously like lipgloss. Treat it with caution.
Stick to the traditional healthy vegetable oils and fats like olive, coconut , and melted butter, and you are more likely to actually improve your health.
What you probably didn't hear is that a study published in the British Medical Journal (BMJ) February of this past year found that though the first claim is true--swapping out saturated fats for vegetable oils will lower your cholesterol--if the oil you use instead of saturated fat is full of omega-6 fatty acid, like safflower oil or corn oil, the second claim is completely false.
The study found that when men who had already had a heart attack replaced saturated fats with safflower oil and ate margarine made with safflower oil they significantly raised the risk that they would die of a heart attack, stroke or, in fact, any cause of death, over the next five years.
How significantly was that risk raised? The study states: "Among the control and intervention groups combined, an increase of 5% of food energy from unspecified PUFA [polyunsaturated fatty acids] predicted about 30% higher risk of cardiovascular death and all cause mortality.
A reduction in SFA [saturated fat] and increase in the PUFA:SFA ratio were also associated with increased risks of all cause and cardiovascular mortality." In short, the more they replaced saturated fat with "healthy" polyunsaturated oil the more likely they were to die.
I was only made aware of this study last week, when the Canadian Medical Association Journal (CMAJ) published an opinion piece questioning whether the government should be putting "heart healthy" labels on corn oil and other polyunsaturated fats. (Details HERE.) They cited the February BMJ study in their write-up.
What doesn't come across in the small amount of press the CMAJ article got is something that makes the BMJ study even more significant: The data that this finding was based on was 40 years old. It was collected during the Sydney Diet Heart Study, a randomized controlled trial conducted in 1966-73.
This was one of the many landmark interventional studies whose result was used to convince doctors that replacing saturated fats with polyunsaturated fats would lower cholesterol and, by implication, prevent heart disease.
But while the authors of the original study published the finding that the polyunsaturated fats would lower both cholesterol and triglycerides, they did not look to see whether lowering cholesterol with this intervention actually helped prevent heart-related deaths.
They eventually admitted in a study published in 1978--a full 5 years after they began to publish their results--that there was a higher "all cause mortality" in the group eating the safflower oil, but they did not look at whether these deaths were from cardiovascular-related causes. This was a surprising omission, given the point of the dietary intervention--to lower cholesterol in order to prevent heart attacks.
So it was only in the last few years that a new group of researchers were able to go back to the original study's raw data and take another look at it. When they did so, they discovered what they term "previously missing data." This "missing data" was the data that led to the conclusion that there was a 30% greater risk of cardiovascular death among the people in the study who ate the cholesterol-lowering oil.
Getting at this missing data was not a trivial process. The original study data had been stored on 9-track tape--the kind you can see at left--which used to be used by IBM 360 series mainframe computers. There are only a very few data recovery specialists around who can still read these kinds of tapes.
Once they recovered the data, the researchers did a very careful analysis, teasing out other factors that might have affected the death rate and, most significantly, analyzing whether the transfat associated with the margarine the test subjects ate might have explained the higher death rate. They conclude it did not.
They also point out that this re-analysis of the data echoes what was found in two other re-analyses of 1960-70s era cholesterol/heart diet trials: Linoleic acid, with its high proportion of Omega-6 fatty acid and complete lack of Omega-3 fatty acid is really toxic stuff.
You can read the whole BMJ study here:
Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.
Omega-6 Fatty Acids Promote Inflammation
The researchers believe that the reason that the polyunsaturated oils used in these cholesterol-lowering diets were so toxic was because the vegetable oils used were very high in Linoleic Acid, an Omega-6 fatty acid, and devoid of the countervailing Omega-3 fatty acids you need to consume to keep Omega-6 fatty acids from promoting inflammation.
So, okay. Safflower oil is now out of your diet. But it turns out that safflower oil is not the only common vegetable oil that is rich in linoleic oil. Corn oil is very high in it, too. You can see a complete list of oils sorted by their percentage of Linoleic acid HERE.
Finally, though health nuts who still fear that eating saturated fat will kill them will tell you that canola oil and flaxseed oil are healthier alternatives, neither of these oils has been a part of the human diet for any significant period of time the way animal and dairy fats have been.
Canola oil does contain Omega-3 fatty acids, but the process used to take away its rank smell and keep it from going rancid is likely to damage them. Damaged Omega-3 oils is not healthy. Flaxseed oil is the recently renamed stuff we used to call linseed oil and use for mixing up oil based paint--which it often tastes like. It's safe to eat if you keep it refrigerated and don't let it go rancid, but since it is not a traditional food, I would suggest eating it in small quantities.
Palm oil is another fat that has recently made its way into our food system, as manufacturers are using it as a replacement for the hydrogenated oils full of transfat. But while there may be health benefits from consuming the palm oil eaten in traditional societies, the industrially processed palm oil that is appearing on supermarket shelves is very different stuff and may very well be harboring transfat-like molecules that escape the FDA labeling requirements. And besides that, it often tastes--and refuses to melt--suspiciously like lipgloss. Treat it with caution.
Stick to the traditional healthy vegetable oils and fats like olive, coconut , and melted butter, and you are more likely to actually improve your health.
October 1, 2013
Study Quantifies Whether Weight Loss Surgery Cures Diabetes
A study recently published in the Annals of Surgery gives much more insight into oft-repeated claims that weight loss surgery cures diabetes.
The study can be found here:
Can Diabetes Be Surgically Cured? Long-Term Metabolic Effects of Bariatric Surgery in Obese Patients with Type 2 Diabetes Mellitus. Brethauer, Stacy A. et al. Annals of Sugery, 10/13/2013. doi: 10.1097/SLA.0b013e3182a5034b
The study followed 217 people with Type 2 Diabetes who had had weight loss surgery for a period lasting between 5 and 9 years. One hundred and sixty-two had the radical Roux-en-Y gastric bypass operation, which irreversibly reroutes the path of food through the stomach and small intestine. Thirty-two had the potentially reversible gastric banding procedure where a band limits the site of the stomach, and 23 had the irreversible amputation of part of the stomach sleeve known as sleeve gastrectomy.
Complete remission--i.e. a cure--was defined as the patient having an A1C less than 6% and a fasting blood glucose less than 100 mg/dL while taking no diabetic medications.
It is worth noting that many people with Type 2 are able to achieve these same numbers by cutting down their carbohydrate intake, without exposing themselves to any of the significant long-term risks that come with these major surgical interventions.
The Long Term Results
Only 24% of those who had these surgeries met the definition of "complete remission." This, of course, means that 76% still had abnormal blood sugars.
Thirty-four percent were described as having "improved." The study defined "improvemetn" as meaning that the subjects experienced a drop in A1c greater than 1%. Since the starting A1cs of the subjects in this study ranged up to 8.5%, a person could be considered "improved" if their A1c six years after surgery was still 7.25%--a level corresponding to an average blood sugar of 162 mg/dl (9 mmol/L). That is a level high enough to cause all the classic diabetic complications and it correlates with a greatly increased risk of heart attack.
But it gets worse. A full 16% of those who had these major surgeries--one out of 6--saw no improvement at all in their blood sugars.
And even more depressing for people who had these expensive, dangerous surgeries, of those whose blood sugars normalized right after surgery, 19% saw their blood sugars go back up into the diabetic range.
The authors of the study describe these results as being wonderful news showing that "Bariatric surgery can induce a significant and sustainable remission" in people with Type 2 Diabetes.
The statistics above suggest that the improvements caused by these surgeries are almost entirely due to the fact that they make it impossible--at least for a short time after surgery--for people who have rearranged their stomaches to eat any significant amount of the carbohydrate-rich foods that raise the blood sugar of people with diabetes.
As time goes by people who have had some of these procedures will have their stomachs stretch out again and will once again be able to eat the high carbohydrate foods that raise blood sugars, explaining the failure that often occurs in people who at first appeared succesesful.
This is because most people with Type 2, even those with very high A1cs will see dramatic drops in their blood sugars within a week or two if they cut back dramatically on their carbohydrate intake--whether they do this by limiting their stomach size or changing what they keep in the refrigerator.
Those who don't see a drop in their blood sugars after restricting carbohydrates usually turn out to have a problem secreting insulin. If they have this kind of surgery they are likely to end up in that unfortunate 16% who get no benefit from it at all. In fact, what they need is not surgery, it's often an appropriately prescribed insulin regimen.
But sadly, rarely do surgeons or the doctors who refer people for this surgery do the tests that could determine if people are insulin deficient and hence unlikely to benefit from this kind of surgery.
Finally, it is interesting that there is no hint here to confirm the latest, most fashionable explanation for why weight loss surgery works--that rearranging the gut boosts incretin hormones and lowers blood sugar independent of carbohydrate intake.
Why No Mention of the Complication Rate?
A far worse omission, however, is that this study omits any mention of the surgical complications these people could have suffered as a result of undergoing these major invasive surgeries. Quite a few studies have found that the rate of post-operative complications associated with these surgeries is between 7 and 9%--almost one in ten.
Serious complications--such as incisions opening-occur in roughly 3.5%--one in 29--and one in a hundred patients require additional surgeries. (Details HERE and HERE) Even more tragic, large epidemiological studies find that something like .18% of patients who have these surgeries die. That is almost two per thousand. Given that it is estimated that 205,000 people a year have weight loss surgery, this works out to about 400 deaths each year due entirly to elective bariatric surgery.
And these complication statistics include only the deaths and complications that occur shortly after surgery. They ignore the ongoing health problems that many people suffer after having supposedly "successful" surgeries.
These problems include permanent malnutrition due to the loss of the gut's ability to absorb vital minerals and mental changes which can lead to fatal anorexia or an increased incidence of suicide. I have heard from several people whose relatives died from the anorexia and malnutrition caused by having had this kind of surgery. It is a real problem which probably has something to do with changes the surgery makes in the gut hormones that regulate appetite and feeding behavior in the brain.
Consider the Alternatives
So before you sign up for this questionable diabetes cure, it's worth checking out the alternatives. Because the surgeons selling these expensive surgeries don't tell you that the majority of people with Type 2 diabetes can achieve the exact same kind long term results as are depicted in this study--or better--without resorting to surgery. They can do it simply by following the technique described here:
How to Lower Your Blood Sugar
It is carbohydrates that raise blood sugar, and cutting back on them will lower the blood sugar of most people with Type 2 Diabetes.
But despite this being true, many people who are told that they can lower their blood sugar permanently by cutting down on their carbohydrate intake dismiss this idea saying, "I could never stop eating the high carb foods I love."
If you fall into that category and would prefer a surgical approach, it's worth considering that any weight loss surgery that lowers your blood sugar will force you to give up those high carb foods forever. When your stomach is shrunken to where you can only eat 1000 or so calories a day, it is physically impossible to eat a lot of carbohydrates .And in many cases--often those who are most "successful" with both weight loss and blood sugar control, the changes the surgery makes in your digestive tract ensure that high carbohydrate foods will cause projectile vomiting--an experience that will quickly train you to avoid the foods that could raise your blood sugar no matter how you used to feel about them.
Personally, I'd prefer to lower my blood sugar using a technique that doesn't expose me to the risk of death or permanent malnutrition and that allows me an occasional indulgence in ordinary foods. I also prefer an approach that doesn't permanently rearrange my organs and which leaves open the possibility that I might be able to benefit from some less radical future advance in the control of Type 2 diabetes.
There is a lot of money in selling these surgeries. And as everyone with diabetes knows, it is the money to be made that drives what treatments we are directed to. Surgeons market their surgeries to your family doctors just as much as the drug companies market their latest, most expensive, and most dangerous drugs. I hear from quite a few people whose family doctors have told them to have these surgeries--without ever suggesting carb restricted diets or doing the tests needed to determine if the person needs insulin.
But armed with the facts like those that came out of this study, you will be better prepared to defend yourself against inappropriate and potentially harmful treatments.
One last note: It continues to amaze me that the same physicians who continue to issue dire warnings about how dangerous low carb diets are to your health are the same people who recommend these far more dangerous surgeries.
When researching my book Diet 101: The Truth about Low Carb Diets I was able to find a grand total of 2 verified reports of deaths that could be linked in any way with low carb dieting--and they were linked with starvation diets that were dangerous not because of their low carbohydrate intake but because of their lack of calories and electrolytes. Compare this with those 400 deaths a year attributable to these surgeries!
The study can be found here:
Can Diabetes Be Surgically Cured? Long-Term Metabolic Effects of Bariatric Surgery in Obese Patients with Type 2 Diabetes Mellitus. Brethauer, Stacy A. et al. Annals of Sugery, 10/13/2013. doi: 10.1097/SLA.0b013e3182a5034b
The study followed 217 people with Type 2 Diabetes who had had weight loss surgery for a period lasting between 5 and 9 years. One hundred and sixty-two had the radical Roux-en-Y gastric bypass operation, which irreversibly reroutes the path of food through the stomach and small intestine. Thirty-two had the potentially reversible gastric banding procedure where a band limits the site of the stomach, and 23 had the irreversible amputation of part of the stomach sleeve known as sleeve gastrectomy.
Complete remission--i.e. a cure--was defined as the patient having an A1C less than 6% and a fasting blood glucose less than 100 mg/dL while taking no diabetic medications.
It is worth noting that many people with Type 2 are able to achieve these same numbers by cutting down their carbohydrate intake, without exposing themselves to any of the significant long-term risks that come with these major surgical interventions.
The Long Term Results
Only 24% of those who had these surgeries met the definition of "complete remission." This, of course, means that 76% still had abnormal blood sugars.
Thirty-four percent were described as having "improved." The study defined "improvemetn" as meaning that the subjects experienced a drop in A1c greater than 1%. Since the starting A1cs of the subjects in this study ranged up to 8.5%, a person could be considered "improved" if their A1c six years after surgery was still 7.25%--a level corresponding to an average blood sugar of 162 mg/dl (9 mmol/L). That is a level high enough to cause all the classic diabetic complications and it correlates with a greatly increased risk of heart attack.
But it gets worse. A full 16% of those who had these major surgeries--one out of 6--saw no improvement at all in their blood sugars.
And even more depressing for people who had these expensive, dangerous surgeries, of those whose blood sugars normalized right after surgery, 19% saw their blood sugars go back up into the diabetic range.
The authors of the study describe these results as being wonderful news showing that "Bariatric surgery can induce a significant and sustainable remission" in people with Type 2 Diabetes.
The statistics above suggest that the improvements caused by these surgeries are almost entirely due to the fact that they make it impossible--at least for a short time after surgery--for people who have rearranged their stomaches to eat any significant amount of the carbohydrate-rich foods that raise the blood sugar of people with diabetes.
As time goes by people who have had some of these procedures will have their stomachs stretch out again and will once again be able to eat the high carbohydrate foods that raise blood sugars, explaining the failure that often occurs in people who at first appeared succesesful.
This is because most people with Type 2, even those with very high A1cs will see dramatic drops in their blood sugars within a week or two if they cut back dramatically on their carbohydrate intake--whether they do this by limiting their stomach size or changing what they keep in the refrigerator.
Those who don't see a drop in their blood sugars after restricting carbohydrates usually turn out to have a problem secreting insulin. If they have this kind of surgery they are likely to end up in that unfortunate 16% who get no benefit from it at all. In fact, what they need is not surgery, it's often an appropriately prescribed insulin regimen.
But sadly, rarely do surgeons or the doctors who refer people for this surgery do the tests that could determine if people are insulin deficient and hence unlikely to benefit from this kind of surgery.
Finally, it is interesting that there is no hint here to confirm the latest, most fashionable explanation for why weight loss surgery works--that rearranging the gut boosts incretin hormones and lowers blood sugar independent of carbohydrate intake.
Why No Mention of the Complication Rate?
A far worse omission, however, is that this study omits any mention of the surgical complications these people could have suffered as a result of undergoing these major invasive surgeries. Quite a few studies have found that the rate of post-operative complications associated with these surgeries is between 7 and 9%--almost one in ten.
Serious complications--such as incisions opening-occur in roughly 3.5%--one in 29--and one in a hundred patients require additional surgeries. (Details HERE and HERE) Even more tragic, large epidemiological studies find that something like .18% of patients who have these surgeries die. That is almost two per thousand. Given that it is estimated that 205,000 people a year have weight loss surgery, this works out to about 400 deaths each year due entirly to elective bariatric surgery.
And these complication statistics include only the deaths and complications that occur shortly after surgery. They ignore the ongoing health problems that many people suffer after having supposedly "successful" surgeries.
These problems include permanent malnutrition due to the loss of the gut's ability to absorb vital minerals and mental changes which can lead to fatal anorexia or an increased incidence of suicide. I have heard from several people whose relatives died from the anorexia and malnutrition caused by having had this kind of surgery. It is a real problem which probably has something to do with changes the surgery makes in the gut hormones that regulate appetite and feeding behavior in the brain.
Consider the Alternatives
So before you sign up for this questionable diabetes cure, it's worth checking out the alternatives. Because the surgeons selling these expensive surgeries don't tell you that the majority of people with Type 2 diabetes can achieve the exact same kind long term results as are depicted in this study--or better--without resorting to surgery. They can do it simply by following the technique described here:
How to Lower Your Blood Sugar
It is carbohydrates that raise blood sugar, and cutting back on them will lower the blood sugar of most people with Type 2 Diabetes.
But despite this being true, many people who are told that they can lower their blood sugar permanently by cutting down on their carbohydrate intake dismiss this idea saying, "I could never stop eating the high carb foods I love."
If you fall into that category and would prefer a surgical approach, it's worth considering that any weight loss surgery that lowers your blood sugar will force you to give up those high carb foods forever. When your stomach is shrunken to where you can only eat 1000 or so calories a day, it is physically impossible to eat a lot of carbohydrates .And in many cases--often those who are most "successful" with both weight loss and blood sugar control, the changes the surgery makes in your digestive tract ensure that high carbohydrate foods will cause projectile vomiting--an experience that will quickly train you to avoid the foods that could raise your blood sugar no matter how you used to feel about them.
Personally, I'd prefer to lower my blood sugar using a technique that doesn't expose me to the risk of death or permanent malnutrition and that allows me an occasional indulgence in ordinary foods. I also prefer an approach that doesn't permanently rearrange my organs and which leaves open the possibility that I might be able to benefit from some less radical future advance in the control of Type 2 diabetes.
There is a lot of money in selling these surgeries. And as everyone with diabetes knows, it is the money to be made that drives what treatments we are directed to. Surgeons market their surgeries to your family doctors just as much as the drug companies market their latest, most expensive, and most dangerous drugs. I hear from quite a few people whose family doctors have told them to have these surgeries--without ever suggesting carb restricted diets or doing the tests needed to determine if the person needs insulin.
But armed with the facts like those that came out of this study, you will be better prepared to defend yourself against inappropriate and potentially harmful treatments.
One last note: It continues to amaze me that the same physicians who continue to issue dire warnings about how dangerous low carb diets are to your health are the same people who recommend these far more dangerous surgeries.
When researching my book Diet 101: The Truth about Low Carb Diets I was able to find a grand total of 2 verified reports of deaths that could be linked in any way with low carb dieting--and they were linked with starvation diets that were dangerous not because of their low carbohydrate intake but because of their lack of calories and electrolytes. Compare this with those 400 deaths a year attributable to these surgeries!
September 18, 2013
Generic test strips that work in Ultra meters. Get them before their maker is forced out of business!
UPDATE: May 12, 2014
The FDA issued a warning about Genstrips, telling people not to use them as they are not accurate and the company making them failed quality inspections. Reviewers on Amazon also report that while the strips they purchased earlier worked well, as did mine, the newer ones did not.
http://www.fda.gov/medicaldevices/safety/alertsandnotices/ucm395180.htm
ORIGINAL POST
I learned about the generic One Touch Ultra strips sold as Genstrips in a tweet from diabetes business analyst Scott Strumello (@sstrumello). It turns out that the company that sells them came up with their own strip engineering design that works with the One Touch Ultra meters without violating Johnson & Johnson's patents.
The FDA required rigorous testing before allowing them to be sold, and they passed.
The company then made a deal with Walmart, which would have sold these cheap but effective strips to people all over the world who can't afford the obscene prices Johnson & Johnson charges for them. But Johnson & Johnson hit the company with expensive lawsuits intended to drive them out of business, even though the Patent Bureau has opined that these strips do not violate Johnson & Johnson's patents.
In the face of this legal pressure, Walmart bowed out, so for now the only place you can get them is on Amazon.
You can find the link to buy them here:
Genstrip Test Strips 50ct for Use with Onetouch® Ultra® Meters
Since Johnson & Johnson has vast financial resources they can continue to harass the company that makes Genstrips with lawsuits. The company is financially strapped without significant sales of its strips, and is likely to give up when the money runs out, even if it is in the right, legally. So it may be only a matter of time until the maker of Genstrips goes belly up and Johnson & Johnson is left to enjoy its monopoly. Stockholders will applaud, and the only people who suffer are the 99% who can't afford to shell out hundreds every month to test their blood sugar, even when they need to.
For Use with Old Minis Only?
The documentation with these strips says they should only be used with meters sold before 2010. However, there is a comment on the Amazon page from someone who says this is not true. My testing suggests they are correct.
Apparently the issue is that your meter has to be able to be set to match the code that comes on the vial of strips. All the brand name Ultra strips sold now are coded 25, so you don't ever have to change the code with a newer One Touch Ultra meters, and it is possible that some of them might not allow you to do this.
My Genstrip strips were coded 13, but both an old Ultra Mini meter that was sent to me as a freebie when the Ultra Minis first came out and a brand new Ultra Mini I just bought allowed me to change the meter's code to match that of the strips.
If you are using another brand of Ultra meter, before you buy these strips, make sure your meter lets you change the code. And if you have gotten out of the habit of checking the code on your strips, remember to do it with these. If you don't set the code on your meter, the strips will give an inaccurate reading.
My Tests So Far
I bought a pack and tested them with both my original Mini, which I was sent as a freebie when the Ultra Minis were first released and with a brand new Mini which I received recently from my insurer.
I was not able to test the two Ultra Mini meters simultaneously as I only had one working battery, so there was a time lapse of about ten minutes between the tests of the two meters as I swapped out the battery from the new one to the old one.
I did run a test using the same drop of blood to compare the Genstrip in my brand new Mini with my Freestyle Lite. The Genstrip read 93, the Freestyle 95, and the Mini using the brand name strips read 99. When I got the old Mini working, ten minutes later, it read 99, too.
The Genstrip strip took a fraction of a second longer to fill with blood than the brand name Ultra strip but my meter didn't seem to notice any difference between the two strips.
Given the general unreliability of all meters and strips, I came away feeling confident that the Gentest strips are good enough. I would just as soon buy these strips priced at $18.50 per 50 instead of the obscenely expensive brand name strips.
While they last, these strips might be a better choice than ordering name brand strips from no-name vendors who may sell you heat damaged or out-of-date strips that still cost more than these do.
By the way, if you are wondering what the best way to use your limited supply of any blood sugar test strip might be, please read this page:
How to Lower Your Blood Sugar.
It will teach you how to use the readings you get after meals to tweak your diet until you find one that gives you normal or near normal blood sugars. This approach has worked for thousands of people and it can work for you, too.
The FDA issued a warning about Genstrips, telling people not to use them as they are not accurate and the company making them failed quality inspections. Reviewers on Amazon also report that while the strips they purchased earlier worked well, as did mine, the newer ones did not.
http://www.fda.gov/medicaldevices/safety/alertsandnotices/ucm395180.htm
ORIGINAL POST
I learned about the generic One Touch Ultra strips sold as Genstrips in a tweet from diabetes business analyst Scott Strumello (@sstrumello). It turns out that the company that sells them came up with their own strip engineering design that works with the One Touch Ultra meters without violating Johnson & Johnson's patents.
The FDA required rigorous testing before allowing them to be sold, and they passed.
The company then made a deal with Walmart, which would have sold these cheap but effective strips to people all over the world who can't afford the obscene prices Johnson & Johnson charges for them. But Johnson & Johnson hit the company with expensive lawsuits intended to drive them out of business, even though the Patent Bureau has opined that these strips do not violate Johnson & Johnson's patents.
In the face of this legal pressure, Walmart bowed out, so for now the only place you can get them is on Amazon.
You can find the link to buy them here:
Genstrip Test Strips 50ct for Use with Onetouch® Ultra® Meters
Since Johnson & Johnson has vast financial resources they can continue to harass the company that makes Genstrips with lawsuits. The company is financially strapped without significant sales of its strips, and is likely to give up when the money runs out, even if it is in the right, legally. So it may be only a matter of time until the maker of Genstrips goes belly up and Johnson & Johnson is left to enjoy its monopoly. Stockholders will applaud, and the only people who suffer are the 99% who can't afford to shell out hundreds every month to test their blood sugar, even when they need to.
For Use with Old Minis Only?
The documentation with these strips says they should only be used with meters sold before 2010. However, there is a comment on the Amazon page from someone who says this is not true. My testing suggests they are correct.
Apparently the issue is that your meter has to be able to be set to match the code that comes on the vial of strips. All the brand name Ultra strips sold now are coded 25, so you don't ever have to change the code with a newer One Touch Ultra meters, and it is possible that some of them might not allow you to do this.
My Genstrip strips were coded 13, but both an old Ultra Mini meter that was sent to me as a freebie when the Ultra Minis first came out and a brand new Ultra Mini I just bought allowed me to change the meter's code to match that of the strips.
If you are using another brand of Ultra meter, before you buy these strips, make sure your meter lets you change the code. And if you have gotten out of the habit of checking the code on your strips, remember to do it with these. If you don't set the code on your meter, the strips will give an inaccurate reading.
My Tests So Far
I bought a pack and tested them with both my original Mini, which I was sent as a freebie when the Ultra Minis were first released and with a brand new Mini which I received recently from my insurer.
I was not able to test the two Ultra Mini meters simultaneously as I only had one working battery, so there was a time lapse of about ten minutes between the tests of the two meters as I swapped out the battery from the new one to the old one.
I did run a test using the same drop of blood to compare the Genstrip in my brand new Mini with my Freestyle Lite. The Genstrip read 93, the Freestyle 95, and the Mini using the brand name strips read 99. When I got the old Mini working, ten minutes later, it read 99, too.
The Genstrip strip took a fraction of a second longer to fill with blood than the brand name Ultra strip but my meter didn't seem to notice any difference between the two strips.
Given the general unreliability of all meters and strips, I came away feeling confident that the Gentest strips are good enough. I would just as soon buy these strips priced at $18.50 per 50 instead of the obscenely expensive brand name strips.
While they last, these strips might be a better choice than ordering name brand strips from no-name vendors who may sell you heat damaged or out-of-date strips that still cost more than these do.
By the way, if you are wondering what the best way to use your limited supply of any blood sugar test strip might be, please read this page:
How to Lower Your Blood Sugar.
It will teach you how to use the readings you get after meals to tweak your diet until you find one that gives you normal or near normal blood sugars. This approach has worked for thousands of people and it can work for you, too.
September 2, 2013
Onlgyza Appears to Raise Risk of Heart Failure
A two year long study of two DPP-4 inhibitors (one not available in the U.S.) found that these drugs did not, as hoped, lower the risk of heart attack in people with diabetes who took them, and they found a surprising increase in cases of heart failure among people taking Onglyza.
UPDATE 2-Doctors get good and bad safety news on diabetes drugs
http://www.reuters.com/article/2013/09/02/heart-diabetes-idUSL6N0GY0S720130902
The study also claimed to find no sign of pancreatic disease with Onglyza, but there are several reasons to discount this finding:
1. The study only lasted 2 years, which is far too short a time for the changes in pancreatic architecture discovered by Dr. Butler to result in pancreatitis. (Details HERE)
2. Cancers also take much longer than 2 years to cause symptoms. Pancreatic cancer, in particular, is almost always symptom free until it is too late for any treatment to keep the patient from dying within a few months. The patients in Dr. Butler's study who took Januvia and died with small precancerous tumors in their pancreases and abnormal cells throughout the pancreatic tissue had no symptoms suggesting anything was wrong with them.
The British Medical Journal looked into this issue and found disturbing signs of suppression of evidence suggesting this is a very real problem: Their findings are discussed here: Medcscape: BMJ Digs Deep Into Incretins and Pancreatic Cancer Debate.
The actual BMJ review article is found here:
Has pancreatic damage from glucagon suppressing diabetes drugs been underplayed?
The chances are very good that it will take 10 years or more for the pancreatic tumors these drugs are capable of growing to cause the epidemic of cancer deaths that I fear is coming. By the time the deaths appear, it will be too late to do anything.
Please do not take or let anyone you love take any of the incretin drugs. There is a lot of money going into studies like this that are supposed to reassure patients and keep the money machine cranking for the companies that sell these highly profitable drugs. But there is enough evidence, despite the white washes that these drugs are dangerous that there is no reason to take any of them.
No matter how bad your blood sugar might be, a combination of lower carb diet and, if needed insulin, properly dosed (which, alas, it often isn't) will lower your blood sugar far more safely.
UPDATE 2-Doctors get good and bad safety news on diabetes drugs
http://www.reuters.com/article/2013/09/02/heart-diabetes-idUSL6N0GY0S720130902
The study also claimed to find no sign of pancreatic disease with Onglyza, but there are several reasons to discount this finding:
1. The study only lasted 2 years, which is far too short a time for the changes in pancreatic architecture discovered by Dr. Butler to result in pancreatitis. (Details HERE)
2. Cancers also take much longer than 2 years to cause symptoms. Pancreatic cancer, in particular, is almost always symptom free until it is too late for any treatment to keep the patient from dying within a few months. The patients in Dr. Butler's study who took Januvia and died with small precancerous tumors in their pancreases and abnormal cells throughout the pancreatic tissue had no symptoms suggesting anything was wrong with them.
The British Medical Journal looked into this issue and found disturbing signs of suppression of evidence suggesting this is a very real problem: Their findings are discussed here: Medcscape: BMJ Digs Deep Into Incretins and Pancreatic Cancer Debate.
The actual BMJ review article is found here:
Has pancreatic damage from glucagon suppressing diabetes drugs been underplayed?
The chances are very good that it will take 10 years or more for the pancreatic tumors these drugs are capable of growing to cause the epidemic of cancer deaths that I fear is coming. By the time the deaths appear, it will be too late to do anything.
Please do not take or let anyone you love take any of the incretin drugs. There is a lot of money going into studies like this that are supposed to reassure patients and keep the money machine cranking for the companies that sell these highly profitable drugs. But there is enough evidence, despite the white washes that these drugs are dangerous that there is no reason to take any of them.
No matter how bad your blood sugar might be, a combination of lower carb diet and, if needed insulin, properly dosed (which, alas, it often isn't) will lower your blood sugar far more safely.
August 14, 2013
Berberine Works But May Very Well Be Harmful
I have been getting a lot of email of late about the supplement Berberine, which appears to be the latest miracle cure being sold to those people with diabetes who believe that completely unregulated herbs imported from countries with long histories of food and drug adulteration are somehow safer and "more natural" than the tightly regulated pharamceuticals.
Berberine does appear to work to lower blood sugar. The problem is that we really know very little about how it does it or what its long term effects are on the body. I see many mentions on sites promoting berberine supplements of the fact that berberine has a long history of use in Chinese medicine. However, quite a few of the traditional Chinese herbs have turned out to be highly toxic, and it's worth noting that the incidence of kidney and other urinary tract cancer among Chinese herbalists is far greater than that of the population at large. (Details HERE)
You can lower blood sugar by damaging your liver as happens with severe alcoholism. You can lower blood sugar with drugs that raise the likelihood of heart attack, as is the case with most sulfonylurea drugs. (Details HERE) You can lower blood sugar with drugs that over time damage the pancreas as is the case with the incretin drugs.(Details HERE) And you can lower blood sugar by taking drugs that turn bone precursor cells into fat cell, as happens with Avandia and Actos, which, over a decade of use of these drugs can lead to your developing bones so brittle that they are prone to breaking. (Details HERE)
Many of these severe, life-ruining side effects did not show up until people had taken these drugs for five to ten years. So the fact that a drug lowers blood sugar for three months in a small population without major harm tells you nothing about its actual safety.
To get a feel for the quality of the research supporting the claims about berberine, scroll down to the Reference section of this page: http://examine.com/supplements/Berberine/ .
Ignore the enthusiastic editorializing by the editors of the site who don't know very much about diabetes or the drugs that berberine is being compared to and pay attention to the quality of the journals publishing these studies. Most are very obscure. Some sound like they are one of the many "pay to play" journals beloved by supplement sellers--journals that will publish anything as long as they are paid a hefty fee.
Those studies on berberine published in respected endocrinology journals involve small groups of people taking the drug for very short periods. The only one I could find with a large number of subjects is a meta analysis where data from 14 different very small studies was pooled. Meta analyses are only as good as the quality of the underlying studies, which in this case is not very good.
Some studies published in quality journals suggest that berberine's positive effects may stem from the fact that it activates AMP-Kinase, which is what metformin does. If this is the case, you have to ask yourself, why not just take metformin, a safe, very well understood drug that has been in use since the 1950s and which must meet rigorous manufacturing standards before it is sold.
Several mainstream studies claims to have found that berberine inhibits DPP-4 and raises the concentration of the incretin hormone GLP-1 which is the mechanism used by the incretin drugs Januvia, Onglyza, and Trajenta. As discussed elsewhere, inhibiting DPP-4 can turn off a mechanism the immune system uses to kill cells that have become cancerous, which may make these a poor choice of drug. In addition, accumulating evidence is pointing to the possibility that artificially raising GLP-1 levels over a long period of time leads to the growth of abnormal cells in the pancreas which may grow into the ducts and cause pancreatitis or turn into precancerous tumors. (Details HERE)
Mainstream research also finds that berberine has a significant impact on your liver. Repeated use downregulates several important enzymes (P450 cytochromes ) that the body uses to eliminate drugs. You can read about that here: http://www.ncbi.nlm.nih.gov/pubmed/21870106.
This means that if you are taking berberine, other drugs you take may not be eliminated properly if they use those enzymes and may build up to toxic levels, while others, which require those enzymes to be working so that the drug can be broken down into the active form of the chemical they contain may not work as expected.
In particular you should not combine repaglinide (Prandin) with berberine as that combination may produce hypos since repaglinide is eliminated from the body by an enzyme that berberine inhibits. Since metformin also inhibits one of these enzymes to some extent, combining berberine and metformin is probably a bad idea, too. (Note I have blogged about the combined effect of metformin and prandin HERE).
Other drugs affected by berberine include cyclosporin (Neoral, Sandimmune), lovastatin (Mevacor), clarithromycin (Biaxin), indinavir (Crixivan), sildenafil (Viagra), triazolam (Halcion), and many others.
As always, when you buy an unregulated supplement, you have no way of knowing what is actually in the pill. Herbs grown in third world countries often contain toxic herbicides which are prohibited in the U.S.. And supplements manufactured abroad may also contain lead and other toxic heavy metals, as well as other contaminants. As supplements are completely unregulated in the U.S. and receive no scrutiny unless they kill someone, the assurances of the supplement companies that their supplements are "pure" are worthless. When supplements are taken to the lab by consumer groups, they often turn out to contain different dosages thatn what the label claims and to be contaminated.
With all this in mind, it seems prudent if you are going to use a drug to lower your blood sugar, to stick to drugs that are regulated, provided in pills of known dosage, and which have long track records for safety. Currently, the only drugs that fit that description are: metformin, insulin, prandin, gliclazide (not available in the U.S.) and acarbose.
Berberine does appear to work to lower blood sugar. The problem is that we really know very little about how it does it or what its long term effects are on the body. I see many mentions on sites promoting berberine supplements of the fact that berberine has a long history of use in Chinese medicine. However, quite a few of the traditional Chinese herbs have turned out to be highly toxic, and it's worth noting that the incidence of kidney and other urinary tract cancer among Chinese herbalists is far greater than that of the population at large. (Details HERE)
You can lower blood sugar by damaging your liver as happens with severe alcoholism. You can lower blood sugar with drugs that raise the likelihood of heart attack, as is the case with most sulfonylurea drugs. (Details HERE) You can lower blood sugar with drugs that over time damage the pancreas as is the case with the incretin drugs.(Details HERE) And you can lower blood sugar by taking drugs that turn bone precursor cells into fat cell, as happens with Avandia and Actos, which, over a decade of use of these drugs can lead to your developing bones so brittle that they are prone to breaking. (Details HERE)
Many of these severe, life-ruining side effects did not show up until people had taken these drugs for five to ten years. So the fact that a drug lowers blood sugar for three months in a small population without major harm tells you nothing about its actual safety.
To get a feel for the quality of the research supporting the claims about berberine, scroll down to the Reference section of this page: http://examine.com/supplements/Berberine/ .
Ignore the enthusiastic editorializing by the editors of the site who don't know very much about diabetes or the drugs that berberine is being compared to and pay attention to the quality of the journals publishing these studies. Most are very obscure. Some sound like they are one of the many "pay to play" journals beloved by supplement sellers--journals that will publish anything as long as they are paid a hefty fee.
Those studies on berberine published in respected endocrinology journals involve small groups of people taking the drug for very short periods. The only one I could find with a large number of subjects is a meta analysis where data from 14 different very small studies was pooled. Meta analyses are only as good as the quality of the underlying studies, which in this case is not very good.
Some studies published in quality journals suggest that berberine's positive effects may stem from the fact that it activates AMP-Kinase, which is what metformin does. If this is the case, you have to ask yourself, why not just take metformin, a safe, very well understood drug that has been in use since the 1950s and which must meet rigorous manufacturing standards before it is sold.
Several mainstream studies claims to have found that berberine inhibits DPP-4 and raises the concentration of the incretin hormone GLP-1 which is the mechanism used by the incretin drugs Januvia, Onglyza, and Trajenta. As discussed elsewhere, inhibiting DPP-4 can turn off a mechanism the immune system uses to kill cells that have become cancerous, which may make these a poor choice of drug. In addition, accumulating evidence is pointing to the possibility that artificially raising GLP-1 levels over a long period of time leads to the growth of abnormal cells in the pancreas which may grow into the ducts and cause pancreatitis or turn into precancerous tumors. (Details HERE)
Mainstream research also finds that berberine has a significant impact on your liver. Repeated use downregulates several important enzymes (P450 cytochromes ) that the body uses to eliminate drugs. You can read about that here: http://www.ncbi.nlm.nih.gov/pubmed/21870106.
This means that if you are taking berberine, other drugs you take may not be eliminated properly if they use those enzymes and may build up to toxic levels, while others, which require those enzymes to be working so that the drug can be broken down into the active form of the chemical they contain may not work as expected.
In particular you should not combine repaglinide (Prandin) with berberine as that combination may produce hypos since repaglinide is eliminated from the body by an enzyme that berberine inhibits. Since metformin also inhibits one of these enzymes to some extent, combining berberine and metformin is probably a bad idea, too. (Note I have blogged about the combined effect of metformin and prandin HERE).
Other drugs affected by berberine include cyclosporin (Neoral, Sandimmune), lovastatin (Mevacor), clarithromycin (Biaxin), indinavir (Crixivan), sildenafil (Viagra), triazolam (Halcion), and many others.
As always, when you buy an unregulated supplement, you have no way of knowing what is actually in the pill. Herbs grown in third world countries often contain toxic herbicides which are prohibited in the U.S.. And supplements manufactured abroad may also contain lead and other toxic heavy metals, as well as other contaminants. As supplements are completely unregulated in the U.S. and receive no scrutiny unless they kill someone, the assurances of the supplement companies that their supplements are "pure" are worthless. When supplements are taken to the lab by consumer groups, they often turn out to contain different dosages thatn what the label claims and to be contaminated.
With all this in mind, it seems prudent if you are going to use a drug to lower your blood sugar, to stick to drugs that are regulated, provided in pills of known dosage, and which have long track records for safety. Currently, the only drugs that fit that description are: metformin, insulin, prandin, gliclazide (not available in the U.S.) and acarbose.
July 23, 2013
I'm Taking a Break from Blogging
I'm taking a break from blogging about diabetes news. If something major occurs, I'll blog about it, but I'm not going to be posting minor tidbits anymore.
Almost all the news items I've been highlighting here over the past few months just reiterate some point made in a previous post or add more data to support an argument already fleshed out on the main site.
The 500+ posts already to be found here and the hundreds of pages available at the main site http://bloodsugar101.com have covered just about everything you need to know about Type 2 diabetes, diabetes drugs, and diet.
To find information about a diabetes-related topic use the "Search this Blog and its Cites" link located at the top of the right hand column of this page.
To preserve your health if you have been diagnosed with Type 2 diabetes, just do the following:
1. Learn what blood sugars are truly normal.
2. Learn how blood sugar control works and how it stops working.
3. Learn what blood sugar levels cause diabetic complications and heart disease.
4. Learn how to lower your blood sugar to the safe range using dietary changes.
5. Learn what diabetes drugs are safe and what drugs are dangerous.
6. If you are tempted to try supplements read about what they really do HERE and HERE.
Almost all the news items I've been highlighting here over the past few months just reiterate some point made in a previous post or add more data to support an argument already fleshed out on the main site.
The 500+ posts already to be found here and the hundreds of pages available at the main site http://bloodsugar101.com have covered just about everything you need to know about Type 2 diabetes, diabetes drugs, and diet.
To find information about a diabetes-related topic use the "Search this Blog and its Cites" link located at the top of the right hand column of this page.
To preserve your health if you have been diagnosed with Type 2 diabetes, just do the following:
1. Learn what blood sugars are truly normal.
2. Learn how blood sugar control works and how it stops working.
3. Learn what blood sugar levels cause diabetic complications and heart disease.
4. Learn how to lower your blood sugar to the safe range using dietary changes.
5. Learn what diabetes drugs are safe and what drugs are dangerous.
6. If you are tempted to try supplements read about what they really do HERE and HERE.
July 3, 2013
Final June Diabetes News Snippet Post
Jenny
said...
7:33 AM, June 05, 2013
Chris
said...
8:36 AM, June 05, 2013
Jenny
said...
6:08 PM, June 13, 2013
Jenny
said...
3:15 PM, June 17, 2013
Jenny
said...
9:21 AM, June 20, 2013
Jenny
said...
9:38 AM, June 20, 2013
Jenny
said...
8:42 AM, July 03, 2013
Jenny
said...
The FDA is taking another look at Avandia's relationship to heart disease.
http://www.forbes.com/sites/matthewherper/2013/06/04/battleground-fda-how-tomorrows-avandia-panel-could-help-shape-the-future-of-diabetes/
But whatever they conclude about whether or not Avandia causes heart attacks, we know that it, like Actos, also weakens the bones over time and makes them prone to fracture, since it converts that stem cells that should become bone cells into baby fat cells.
It, like Actos, also raises the chances of experiencing retinal edema--swelling in the blood vessels in your eye that can contribute to blindness.
Finally, both Avandia and Actos have been found to cause heart failure in people who had no symptoms of it before taking the drug. Heart failure is different from heart attack, and refers to weakening of the heart muscle that greatly raises the risk of dying within a few years.
Bottom line. The reasons for reviewing Avandia are all about making money for the drug company. There is NO reason for you to be taking this drug--or for that matter, any other new diabetes drug released over the past 6 years.
Am a diabetes newbie here. My recent diagnosis is associated with my second heart attack in six years. Thank you for writing this blog. I'm looking forward to relying on your pointed references in answer to many of my questions, rather than having to scour a dozen websites.
Scientists find a new medium that allows them to grow ten times the usual number of beta cells in culture. Apparently they are normal cells. This is very good news for those with Type 1 Diabetes who need islet transplants to replace dead beta cells.
Science Daily: Major Hurdle Cleared to Diabetes Transplants
Good news for ordinary people. The Supreme court ruled that the FTC can sue drug companies that pay generic drug companies not to make their patent-expired drugs so that they can continue to price gouge.
Reuters: Supreme court says FTC can sue over deals that delay generic drug sales
Dietary fructose causes liver damage in monkeys fed diets that don't cause weight gain. The damage is associated with bacteria leaking into the liver as the fructose seems to modify characteristics of the digestive tract.
Science Daily: Dietary Fructose Causes Liver Damage in Animal Model
Here's an excellent summary of ALL the studies pointing to serious problems with all the incretin drugs. There are a lot of them from many different kinds of research and they make it crystal clear that the American Diabetes Association's claim that the research is ambiguous is an industry-sponsored lie.
Pharmlot: Troubling New Signals? ? Diabetes Drugs & Adverse Event Reports
A major study published in the journal Science explains why our understanding of how mitochondria works has been wrong.
At the end of a report about the study we learn, "During the study the team also made the unexpected discovery that the most widely used mouse strain for laboratory genetic analysis is unable to correctly assemble the respiratory supercomplexes. This raises serious questions about the validity of extrapolating results obtained with these mice to humans."
This may explain why so much mouse research comes up with findings that aren't true for people, for example, that eating a high fat diet causes diabetes.
Mitochondria are where cells burn fats and sugars, so when they aren't working properly blood sugar and fat metabolism can be skewed.
Science Daily: Researchers Reformulate the Model of Mitochondrial Function
Last week was the annual ADA Scientific Sessions, the big conference where diabetes specialists get together to present research findings and be lobbies by drug and device salesforces.
(I am on the mailing list to get the press releases inviting me to discuss various presentations to be given at the conference, so I get a bunch of mail inviting me to learn more about drug company sponsored crap.)
Nothing that advanced the knowledge of anyone not educated by drug companies seems to have come out of this get together. One study found that losing weight doesn't eliminate heart conditions in people with diabetes. Since they lost weight in ways that did not lower their blood sugar below the 150 mg/dl level that solid research links to heart conditions, this did not amaze me, but it was news to doctors. Unfortunately, it is likely to make them prescribe more weight loss surgery which by its nature makes people cut carbs way, way down and can have positive effects on blood sugar.(If it doesn't kill you or leave you nutritionally compromised for life.)
Another study found that eating a low carb diet lowers blood sugar much more than eating a low fat/low cal diet. (We knew that, didn't we?)
I am pretty burnt out on following diabetes research because after 15 years it has become evident that doctors will never pay attention to anything that doesn't enrich drug or device surgeons, or perhaps surgeons--very well funded groups that profit from the suffering of people with diabetes. That it is news that cutting carbs lowers blood sugars 20 years after Dr. Bernstein published on the same subject shows you what we are up against.
And the complete lack of curiosity of doctors, who sheeplike follow whatever they are told by the industry "Thought leaders, a fancy term for " doctors who are paid hundreds of thousands or more by the drug companies to promote their most recent most profitable drugs, ensures nothing will change.
We could cure diabetes were it not that 98% of all research money goes into studies of drugs that counteract symptoms without addressing the cause of those symptoms, and if were not that drug companies would go out of business if we did cure it. It's a 100 billion dollar business making pills and shots that cost $300+ a month which have to be taken every day for decades. Diabetes is the single most widespread costly condition affecting older people.
You'd get fired if you worked for a drug company and came up with anything that actually cured diabetes and your research would go right into the shredder.
June 20, 2013
Major Breakthrough in Using Stem Cells to Cure A Genetic Form of Diabetes
A study just published in the Journal of Clinical Investigation describes what sounds like a very important advance in the treatment of genetically-caused diabetes.
The study is iPSC-derived β cells model diabetes due to glucokinase deficiency. Haiqing Hua et. al Journal of Clinical Investigation, 2013; DOI: 10.1172/JCI67638
To better understand what was done here, read Science Daily: Researchers Demonstrate Use of Stem Cells to Analyze Causes, Treatment of Diabetes
The particular form of diabetes that was studied here was MODY-2. This is a monogentic genetic form of diabetes, which means you need have only one copy of the gene to experience its symptoms. MODY-2 involves the glucokinase gene (GCK) which is often described as a "glucose thermostat." It affects the control of fasting blood sugar, and when it is broken people have diabetic-level fasting blood sugars that, in theory, can not be lowered.
This it turns out, is not entirely true. I have heard from several people diagnosed via gene tests with MODY-2 who report that cutting carbs does lower their fasting blood sugar, even though they were told it would not. My guess is that while their base fasting blood sugar is higher than normal eating a high carb diet further stresses their blood sugars as it does in people without the defect, so removing the carb-related stress lowers their fasting blood sugar to a level slightly higher than normal, but not nearly as bad as what they experience while eating a high carb diet.
But because their fasting blood sugar is higher than normal from birth, which in most people leads to post-meal blood sugars that are also higher than normal, People with this gene often die of heart attacks at very young ages, which is why, though it doesn't cause the extremely high post meal blood sugars that produce the classic diabetic complications, MODY-2 is still a very serious condition which requires life-long vigilance on the part of those who suffer from it.
What the researchers did in this study was to take skin cells from people with MODY-2 and using the kind of wizardry that stem cell scientists now routinely pull off, use them to create pluripotent stem cells--cells that can become any kind of tissue.
The researchers then, using even more stem cell magic, turned these pluripotent stem cells into beta cells, implanted them into mice, and three months later confirmed that these cells were in fact beta cells that showed the characteristics of MODY-2.
That's already pretty amazing, but the researchers were just getting going. Next the scientists "repaired the GCK mutation using molecular techniques." After doing this, "cells with two restored copies of GCK responded normally to the glucose stress test. Unlike other reported techniques, the researchers' approach efficiently repaired the GCK mutation without introducing any potentially harmful additional DNA."
In short, what they did was create perfectly normal beta cells that would have been immunologically identical to those of the skin cell donors that had repaired the flaw that gave these people MODY-2 diabetes. If this is really the case, it should eventually be possible to grow a significant number of these new, repaired beta cells and transplant them back into the people with MODY-2 where they would be able to respond like normal beta cells, secreting insulin when exposed to rising glucose levels. Best of all, these transplants shouldnt require the use of any immunosuppressant drugs.
The part about growing enough cells and transplanting them is still in the future. So even if you have MODY-2 it's going to be a while until there is an actual cure your doctor can prescribe for you. But even so, this is, obviously, extremely good news for anyone who has a genetic form of diabetes which involves damaged beta cells.
And though few people with Type 2 realize it, this would include a lot of people with Type 2, as there are a couple of damaged genes affecting insulin secretion that are very commonly found among Europeans with Type 2 diabetes, for example TCF7L2, which is discussed HERE.
There are other commonly damaged beta cell genes that are found in other ethnic populations too. So in the long run this research could lead to effective beta cell transplants for people with Type 2 that could normalize their blood sugars.
Will it really happen? Hard to say. Sadly, all the money in diabetes treatment lies in creating drugs that have to be taken every day for decades and devices that require very expensive consumable parts that have to be replaced frequently. Since the companies that make those drugs are the companies that fund most research--and the ADA and the JDRF and drive the diabetes research agenda, it may be difficult for the scientists who performed this particular miracle to get the kind of funding it would take to turn beta cell implantation for MODY or Type 2 diabetes into a viable treatment covered by insurance.
Still, if you have a genetic form of diabetes, it's good to know that your children might not have to go through what you did, thanks to the advances made in stem cell research today.
NOTE: Don't confuse this research which is in its early stages with the fake claims of the many scammy "stem cell clinics" you will find on the web that claim to cure diabetes (and anything else that ails you) with transfusions of your own stem cells. These slimy weasels prey on people who don't understand science and cure them only of having healthy bank accounts. Ignore them.
The exciting stem cell research that may pay off for people with diabetes is still, like the study discussed here, in the preliminary lab-bench stage which is very far from being something you could have done to your body to heal it. But someday, if we're lucky . . .
The study is iPSC-derived β cells model diabetes due to glucokinase deficiency. Haiqing Hua et. al Journal of Clinical Investigation, 2013; DOI: 10.1172/JCI67638
To better understand what was done here, read Science Daily: Researchers Demonstrate Use of Stem Cells to Analyze Causes, Treatment of Diabetes
The particular form of diabetes that was studied here was MODY-2. This is a monogentic genetic form of diabetes, which means you need have only one copy of the gene to experience its symptoms. MODY-2 involves the glucokinase gene (GCK) which is often described as a "glucose thermostat." It affects the control of fasting blood sugar, and when it is broken people have diabetic-level fasting blood sugars that, in theory, can not be lowered.
This it turns out, is not entirely true. I have heard from several people diagnosed via gene tests with MODY-2 who report that cutting carbs does lower their fasting blood sugar, even though they were told it would not. My guess is that while their base fasting blood sugar is higher than normal eating a high carb diet further stresses their blood sugars as it does in people without the defect, so removing the carb-related stress lowers their fasting blood sugar to a level slightly higher than normal, but not nearly as bad as what they experience while eating a high carb diet.
But because their fasting blood sugar is higher than normal from birth, which in most people leads to post-meal blood sugars that are also higher than normal, People with this gene often die of heart attacks at very young ages, which is why, though it doesn't cause the extremely high post meal blood sugars that produce the classic diabetic complications, MODY-2 is still a very serious condition which requires life-long vigilance on the part of those who suffer from it.
What the researchers did in this study was to take skin cells from people with MODY-2 and using the kind of wizardry that stem cell scientists now routinely pull off, use them to create pluripotent stem cells--cells that can become any kind of tissue.
The researchers then, using even more stem cell magic, turned these pluripotent stem cells into beta cells, implanted them into mice, and three months later confirmed that these cells were in fact beta cells that showed the characteristics of MODY-2.
That's already pretty amazing, but the researchers were just getting going. Next the scientists "repaired the GCK mutation using molecular techniques." After doing this, "cells with two restored copies of GCK responded normally to the glucose stress test. Unlike other reported techniques, the researchers' approach efficiently repaired the GCK mutation without introducing any potentially harmful additional DNA."
In short, what they did was create perfectly normal beta cells that would have been immunologically identical to those of the skin cell donors that had repaired the flaw that gave these people MODY-2 diabetes. If this is really the case, it should eventually be possible to grow a significant number of these new, repaired beta cells and transplant them back into the people with MODY-2 where they would be able to respond like normal beta cells, secreting insulin when exposed to rising glucose levels. Best of all, these transplants shouldnt require the use of any immunosuppressant drugs.
The part about growing enough cells and transplanting them is still in the future. So even if you have MODY-2 it's going to be a while until there is an actual cure your doctor can prescribe for you. But even so, this is, obviously, extremely good news for anyone who has a genetic form of diabetes which involves damaged beta cells.
And though few people with Type 2 realize it, this would include a lot of people with Type 2, as there are a couple of damaged genes affecting insulin secretion that are very commonly found among Europeans with Type 2 diabetes, for example TCF7L2, which is discussed HERE.
There are other commonly damaged beta cell genes that are found in other ethnic populations too. So in the long run this research could lead to effective beta cell transplants for people with Type 2 that could normalize their blood sugars.
Will it really happen? Hard to say. Sadly, all the money in diabetes treatment lies in creating drugs that have to be taken every day for decades and devices that require very expensive consumable parts that have to be replaced frequently. Since the companies that make those drugs are the companies that fund most research--and the ADA and the JDRF and drive the diabetes research agenda, it may be difficult for the scientists who performed this particular miracle to get the kind of funding it would take to turn beta cell implantation for MODY or Type 2 diabetes into a viable treatment covered by insurance.
Still, if you have a genetic form of diabetes, it's good to know that your children might not have to go through what you did, thanks to the advances made in stem cell research today.
NOTE: Don't confuse this research which is in its early stages with the fake claims of the many scammy "stem cell clinics" you will find on the web that claim to cure diabetes (and anything else that ails you) with transfusions of your own stem cells. These slimy weasels prey on people who don't understand science and cure them only of having healthy bank accounts. Ignore them.
The exciting stem cell research that may pay off for people with diabetes is still, like the study discussed here, in the preliminary lab-bench stage which is very far from being something you could have done to your body to heal it. But someday, if we're lucky . . .
Big Changes in the Drug Patent World Are Good News for People with Diabetes
Several days ago the Supreme Court of the U.S. issued a decision saying that the FDA could sue drug companies that paid off generic drug makers to keep them from releasing generic versions of drugs that had gone off patent.
A second decision that may be just as important for controlling the costs of drugs for people with diabetes occurred on June 18, 2013. A U.S. appeals court found the patent on Novo Nordisk's Prandin diabetes drug Prandimet, a combination of Prandin with metformin to be invalid, paving the way for introduction of a generic version of the medicine.
MedCity Newsletter: Novo Nordisk’s diabetes drug patent ruled invalid, door open for generic version
Drug companies have been creating combination drugs with two off patent drugs claiming they are new drugs that deserve new patents. Then they convince doctors to only prescribe the expensive, patented combination drug rather than the separate generics. ("So much more convenient." "More effective!" Both lies, of course.)
This is good news not only because it makes the combo drug cheaper, but because if upheld it will dissuade drug makers from marketing these combo drugs, which are a very poor choice for consumers because they make it impossible to dose the individual components correctly.
Some people need 1000 mg of metformin a day for it to be effective. Some need 1500, and some need 2000. However, if you put 1000 mg of metformin in the same pill with a full dose of Prandin, an insulin secretion stimulator, you have to double the Prandin to double the metformin dose. Doubling Prandin can cause hypos in people who are sensitive to it. So with a combo pill the person is likely to end up with an optimal dose of only one component of the pill.
Two generic prescriptions should be the same cost or, more commonly, cheaper than one patented pill, except for people who have top tier health insurance whose co-pays are low enough that this shouldn't be an issue. Most people with diabetes can handle opening two pill containers and taking two pills if that means they are a) paying less and b) getting more effective doses.
The drug companies are likely to lobby and appeal this one to the top, too, since their failure to come up with effective new drugs drives them to more and more tricks, like bribing generic drug makers or creating these combo pills to keep their expiring patent moneymakers profitable.
A second decision that may be just as important for controlling the costs of drugs for people with diabetes occurred on June 18, 2013. A U.S. appeals court found the patent on Novo Nordisk's Prandin diabetes drug Prandimet, a combination of Prandin with metformin to be invalid, paving the way for introduction of a generic version of the medicine.
MedCity Newsletter: Novo Nordisk’s diabetes drug patent ruled invalid, door open for generic version
Drug companies have been creating combination drugs with two off patent drugs claiming they are new drugs that deserve new patents. Then they convince doctors to only prescribe the expensive, patented combination drug rather than the separate generics. ("So much more convenient." "More effective!" Both lies, of course.)
This is good news not only because it makes the combo drug cheaper, but because if upheld it will dissuade drug makers from marketing these combo drugs, which are a very poor choice for consumers because they make it impossible to dose the individual components correctly.
Some people need 1000 mg of metformin a day for it to be effective. Some need 1500, and some need 2000. However, if you put 1000 mg of metformin in the same pill with a full dose of Prandin, an insulin secretion stimulator, you have to double the Prandin to double the metformin dose. Doubling Prandin can cause hypos in people who are sensitive to it. So with a combo pill the person is likely to end up with an optimal dose of only one component of the pill.
Two generic prescriptions should be the same cost or, more commonly, cheaper than one patented pill, except for people who have top tier health insurance whose co-pays are low enough that this shouldn't be an issue. Most people with diabetes can handle opening two pill containers and taking two pills if that means they are a) paying less and b) getting more effective doses.
The drug companies are likely to lobby and appeal this one to the top, too, since their failure to come up with effective new drugs drives them to more and more tricks, like bribing generic drug makers or creating these combo pills to keep their expiring patent moneymakers profitable.
June 14, 2013
The ADA's "Investigation" of Incretin Drugs is a Gift to the Drug Companies
UPDATE 6/20/2013: Here's an excellent summary of ALL the studies pointing to serious problems with all the incretin drugs. There are a lot of them from many different kinds of research and they make it crystal clear that the American Diabetes Association's claim discussed below that the research about incretin drugs causing pancreatitis and cancers is ambiguous is an industry-sponsored lie.
Pharmlot: Troubling New Signals? Diabetes Drugs & Adverse Event Reports
ORIGINAL POST
You may have heard that the American Diabetes Association (ADA) had called for a review of the incretin drugs--Januvia, Onglyza, Byetta, Victoza, etc.--in response to the recent discovery, which I described HERE, that they cause abnormal patterns of growth within the pancreas of a kind that lead to both pancreatitis and cancer.
The call for review can be read HERE.
Sadly, this call for review has nothing to do with protecting people with diabetes, a group for whom the ADA has never had much concern, save as a source of contributions to pay the inflated salaries of its top executives.
The ADA is heavily funded by drug manufacturers, and this call for review is an attempt to protect the profits of the companies who make the incretin drugs. That this is the case is made crystal clear in the ADA's call.
They state, "A recent case control trial examining autopsy specimens suggested that exposure to sitagliptin or exenatide in a small number of subjects increased neoplastic changes in the pancreas of subjects with type 2 diabetes to a greater extent than that seen in nondiabetes subjects or diabetic patients treated with drugs other than incretins. This analysis has been criticized from a methodologic standpoint and remains unconfirmed. [emphasis mine]"
This last statement is an out and out lie. The only criticism I have been able to find of Dr. Butler's brilliant study came from a PR flack working for one of the drug companies. Dr. Butler's research validated previous findings in animal research, and it was all the more compelling because though it used "a small number of subjects" taking incretin drugs, every single one of them had abnormal cells, cell growth patterns, and neuroendocrine tumors in thier pancreases after years of taking these drugs--and NONE of the normal people or people with diabetes not taking incretin drugs had these changes or tumors in their pancreases.
The "review" the ADA is calling for, is largely an analysis of previously published research which it believes will show no problems with these drugs. As the ADA's call points out "Administrative database analyses suggest either no effect on pancreatitis or a small risk associated with incretin therapy, but it is less than that due to obesity or alcohol ingestion."
The ADA's specific prescription in the "call" is that, "Independent review of available clinical and pathologic data be conducted. Toward this end, the Association is calling on all pharmaceutical companies with incretin therapies in development or currently marketed to make patient-level data available on all subjects involved in regulatory trials for an independent analysis."
This review is guaranteed to find no problems because, a) the drug company's studies do not include any study of the actual pancreases of the subjects. Remember none of the people autopsied by Dr. Butler's showed ANY symptoms of anything amiss in their pancreases before death. b) The drug company data only covers a brief time period, far too short a period for tumors visible with image technology to develop, or for pancreatitis to occur as a result of abnormal patterns of beta cell growth. c) Drug companies have a long and ugly history of hiding data that might dissuade doctors from prescribing their most profitable drugs, and the incretins are the single most profitable drug category of most of the large drug companies.
So this "review" is guaranteed to find nothing so that the ADA's sponsors can keep selling these highly profitable drugs to every newly diagnosed person with diabetes. But any sense of security the review establishes is delusory, because the highly abnormal cell growth that Dr. Butler found in the pancreases of all the people taking these drugs, who died with no idea that their pancreases had become abnormal, betray the kinds of changes that though they do, eventually kill people, kill people slowly.
Pancreatic tumors are completely undetectable until they reach the point where they are almost universally fatal. They do not show up on scans until they are much larger than the tumors Dr. Butler discovered. So it may take ten years for the abnormal cell growth and small tumors found in the pancreases of people taking incretin drugs to grow to the point where they start killing the people now taking these drugs--the oldest of which, Januvia, has only been on the market for 6.5 years.
Professionals who care about the health of their patients should be calling NOT for "reviews" of existing demographic research, or relying on the drug companies to provide evidence about the drugs' safety. They should be asking why, if these drugs massively enlarge the beta cell mass of people who take them, the blood sugar of people taking incretin drugs continues to be much higher than normal, and, in fact, worsens the longer they take the drugs. (A finding documented by research discussed HERE.)
They should be looking at the glucagon levels in people taking these drugs to see if they are abnormal, which would validate Dr. Butler's finding that the abnormal beta cells grown in response to incretin therapy secrete glucagon not just insulin.
And finally, they should demand that the ADA apologize to Dr. Butler for making completely unsupported attacks on what was a brilliantly conducted, highly technical piece of research.
It won't happen. Instead, this window dressing "review," will find, based on the fact that until now incretins haven't killed enough people to rise to significance, that these drugs are "perfectly safe."
The ADA's press releases will saturate the medical and popular press. Doctors, reassured by the findings of the review will continue to prescribe these drugs to every new patient with diabetes. In another five or six years, when the patents on these highly profitable drugs have expired, the first wave of pancreatic cancer deaths and the pancreatitis epidemic will begin, and they will continue for years to come.
But few will know that these deaths were caused by the incretin drugs. The ADA will assure the public that this wave of deaths is just a terrible, tragic hitherto not understood complication of diabetes, since it has found all the diabetes drugs to be completely safe.
The drug companies will have booked their profits, so they won't care. The ADA's executives who commissioned the study at the request of the drug companies will be enjoying retirements funded by the huge salaries the ADA pays them, or have moved back to their original jobs as highly paid drug company lobbyists.
But you don't have to be one of the victims. If your doctor suggests you take any one of these very worrisome drugs, point your doctor to Dr. Butler's findings (which you will find HERE) and demand that he think critically about any claims of safety made by the ADA's venal flacks.
If you can't normalize your blood sugar by cutting back on carbs and exercising, stick with the safe drugs: Metformin and insulin (and Prandin for those of you who respond very strongly to beta cell stimulation.)
The drugs to watch out for are: Januvia, Janumet, Onglyza, Combiglyze, Victoza, Trajenta, Jentadueto, Byetta, Bydureon, and Victoza. There are more in the pipeline. Any drug whose mechanism involves DPP-4 inhibition or which is a GLP-1 analog falls into the incretin family.
Pharmlot: Troubling New Signals? Diabetes Drugs & Adverse Event Reports
ORIGINAL POST
You may have heard that the American Diabetes Association (ADA) had called for a review of the incretin drugs--Januvia, Onglyza, Byetta, Victoza, etc.--in response to the recent discovery, which I described HERE, that they cause abnormal patterns of growth within the pancreas of a kind that lead to both pancreatitis and cancer.
The call for review can be read HERE.
Sadly, this call for review has nothing to do with protecting people with diabetes, a group for whom the ADA has never had much concern, save as a source of contributions to pay the inflated salaries of its top executives.
The ADA is heavily funded by drug manufacturers, and this call for review is an attempt to protect the profits of the companies who make the incretin drugs. That this is the case is made crystal clear in the ADA's call.
They state, "A recent case control trial examining autopsy specimens suggested that exposure to sitagliptin or exenatide in a small number of subjects increased neoplastic changes in the pancreas of subjects with type 2 diabetes to a greater extent than that seen in nondiabetes subjects or diabetic patients treated with drugs other than incretins. This analysis has been criticized from a methodologic standpoint and remains unconfirmed. [emphasis mine]"
This last statement is an out and out lie. The only criticism I have been able to find of Dr. Butler's brilliant study came from a PR flack working for one of the drug companies. Dr. Butler's research validated previous findings in animal research, and it was all the more compelling because though it used "a small number of subjects" taking incretin drugs, every single one of them had abnormal cells, cell growth patterns, and neuroendocrine tumors in thier pancreases after years of taking these drugs--and NONE of the normal people or people with diabetes not taking incretin drugs had these changes or tumors in their pancreases.
The "review" the ADA is calling for, is largely an analysis of previously published research which it believes will show no problems with these drugs. As the ADA's call points out "Administrative database analyses suggest either no effect on pancreatitis or a small risk associated with incretin therapy, but it is less than that due to obesity or alcohol ingestion."
The ADA's specific prescription in the "call" is that, "Independent review of available clinical and pathologic data be conducted. Toward this end, the Association is calling on all pharmaceutical companies with incretin therapies in development or currently marketed to make patient-level data available on all subjects involved in regulatory trials for an independent analysis."
This review is guaranteed to find no problems because, a) the drug company's studies do not include any study of the actual pancreases of the subjects. Remember none of the people autopsied by Dr. Butler's showed ANY symptoms of anything amiss in their pancreases before death. b) The drug company data only covers a brief time period, far too short a period for tumors visible with image technology to develop, or for pancreatitis to occur as a result of abnormal patterns of beta cell growth. c) Drug companies have a long and ugly history of hiding data that might dissuade doctors from prescribing their most profitable drugs, and the incretins are the single most profitable drug category of most of the large drug companies.
So this "review" is guaranteed to find nothing so that the ADA's sponsors can keep selling these highly profitable drugs to every newly diagnosed person with diabetes. But any sense of security the review establishes is delusory, because the highly abnormal cell growth that Dr. Butler found in the pancreases of all the people taking these drugs, who died with no idea that their pancreases had become abnormal, betray the kinds of changes that though they do, eventually kill people, kill people slowly.
Pancreatic tumors are completely undetectable until they reach the point where they are almost universally fatal. They do not show up on scans until they are much larger than the tumors Dr. Butler discovered. So it may take ten years for the abnormal cell growth and small tumors found in the pancreases of people taking incretin drugs to grow to the point where they start killing the people now taking these drugs--the oldest of which, Januvia, has only been on the market for 6.5 years.
Professionals who care about the health of their patients should be calling NOT for "reviews" of existing demographic research, or relying on the drug companies to provide evidence about the drugs' safety. They should be asking why, if these drugs massively enlarge the beta cell mass of people who take them, the blood sugar of people taking incretin drugs continues to be much higher than normal, and, in fact, worsens the longer they take the drugs. (A finding documented by research discussed HERE.)
They should be looking at the glucagon levels in people taking these drugs to see if they are abnormal, which would validate Dr. Butler's finding that the abnormal beta cells grown in response to incretin therapy secrete glucagon not just insulin.
And finally, they should demand that the ADA apologize to Dr. Butler for making completely unsupported attacks on what was a brilliantly conducted, highly technical piece of research.
It won't happen. Instead, this window dressing "review," will find, based on the fact that until now incretins haven't killed enough people to rise to significance, that these drugs are "perfectly safe."
The ADA's press releases will saturate the medical and popular press. Doctors, reassured by the findings of the review will continue to prescribe these drugs to every new patient with diabetes. In another five or six years, when the patents on these highly profitable drugs have expired, the first wave of pancreatic cancer deaths and the pancreatitis epidemic will begin, and they will continue for years to come.
But few will know that these deaths were caused by the incretin drugs. The ADA will assure the public that this wave of deaths is just a terrible, tragic hitherto not understood complication of diabetes, since it has found all the diabetes drugs to be completely safe.
The drug companies will have booked their profits, so they won't care. The ADA's executives who commissioned the study at the request of the drug companies will be enjoying retirements funded by the huge salaries the ADA pays them, or have moved back to their original jobs as highly paid drug company lobbyists.
But you don't have to be one of the victims. If your doctor suggests you take any one of these very worrisome drugs, point your doctor to Dr. Butler's findings (which you will find HERE) and demand that he think critically about any claims of safety made by the ADA's venal flacks.
If you can't normalize your blood sugar by cutting back on carbs and exercising, stick with the safe drugs: Metformin and insulin (and Prandin for those of you who respond very strongly to beta cell stimulation.)
The drugs to watch out for are: Januvia, Janumet, Onglyza, Combiglyze, Victoza, Trajenta, Jentadueto, Byetta, Bydureon, and Victoza. There are more in the pipeline. Any drug whose mechanism involves DPP-4 inhibition or which is a GLP-1 analog falls into the incretin family.
June 7, 2013
Phosphate Additives Promote Hardening of the Arteries
Several weeks ago I posted about the disturbing link between blood phosphate levels and heart disease, pointing out that people eating low carb diets have a unique exposure to phosphates because they are added to so many of the meats you buy at the grocery store and order in restaurants. In this post I will explain more about what these phospate additives are and why they are so dangerous to our health.
Phosphates are compounds that contain phosphorous and oxygen. They are essential to the construction of every cell in our body as phosphates make up the backbone of DNA, They form essential components in cell membranes and are essential to the proper growth of plants. Adenoside Triphosphate (ATP) is the molecule every cell uses used to store energy. Without it, we're dead meat.
Therefore we get a dose of phosphates any time we eat any meat or vegetable. These are "organic phosphates" which are deeply bound into the structure of the foods we eat--so much so that only 40-60% of the phosphate we consume is actually bioavailable. The rest goes through us undigested.
But these organic are not the phosphates that pose a threat to health. The problem phosphates are the "inorganic phosphates"--chunks of phosphate containing rock--that are added to our foods. The are commonly used as preservatives, flavor additives, and to keep cream from separating in dairy products. Phosphoric acid, which converts to phosphate in our bodies, is added to soda to keep brown sodas from turning jet black, which would make them unappealing to most people. Phosphates are also frequently used to provide the chalky white pill material that holds the supplements you buy in pill form.
Unlike the organic phosphates these inorganic phosphates are 100% bioavailable. That means if you eat 500 mg of calcium phosphate, disodium phosphate, or any of the many other inorganic phosphates added to processed foods or supplements, the whole 500 mg will be absorbed. When it is, it will go into your bloodstream where where will raise your serum phosphate level.
It has long been known that consuming inorganic phosphates can be very dangerous for people with severe kidney disease, as failing kidneys can't remove phosphates from teh blood, and these phosphates precipitate out in the kidney, destroying what little function is left. But while doctors may be aware of this, few of them know that consuming inorganic phosphates also poses a major risk to normal people, because it can promote heart disease.
We know from several well-conducted studies that there is a direct link between serum phosphate level and heart disease. As a recently published review article explains, " Higher serum phosphate levels were independently associated with coronary artery calcification, vascular stiffness, left ventricular hypertrophy, and carotid artery disease, even among individuals with normal kidney function and serum phosphate levels within the normal range."
A study that matched CAC scans to serum phosphate levels verified that rising serum phosphate levels correlated directly to rising Agaston scores in a population who had completely normal kidney function.
The most comprehensive study to investigate the impact of phosphates on heart disease was a study of the Framingham Offspring. It looked at serum phosphate levels in a group of over 3,000 normal people and then looked to see which of them had developed heart disease sixteen years later. It found that:
After reading this, I could not help but wonder if those high serum phosphate levels that caused heart disease were caused by eating diets high in phosphate or whether people destined to get heart disease migh6 have high serum phosphate levels as a side effect of an undiagnosed preexisting health issue.
Could eating a diet high in phosphates be all it took to raise serum phosphate levels? This question was elegantly answered by a study published back in 1977.
In this study subjects who were allowed to eat only the foods supplied by the researchers were, for four weeks, fed a control diet free of any phosphate additives. Then, for the next four weeks, they were fed a diet that contained the identical amount of calories, protein, fat, and carbohydrate as the control diet but this diet was made up of foods containing inorganic phosphate additives, like American cheese, soda, and processed meats.
The report explains, "The average phosphorus content of the daily menu was 979 mg during the control period and 2124 mg during the test period." After a month of eating the foods with the added phosphates, the study participants blood was tested and it was found that they had experienced a dramatic rise in serum phosphates, accompanied by a decrease in serum calcium. The addition of the phosphates to their diets also caused digestive distress to many of the participants--in some cases it persisted throughout the whole study.
When their serum phosphate levels were measured, they were found to have "increased from 3.76 ±0.38 mg/100 ml during the control period to 4.43 ±0.30 mg/ 100 ml [mg/dl] during the high-phosphorus period." This was an 18% rise in serum phosphate level. So yes, upping dietary consumption of inorganic phosphates will raise serum phosphate a lot, even in completely normal people.
And it is also worth noting that the amount of phosphate being consumed by the subjects in this study is likely to be far less than that consumed by the average person today since they were being fed a controlled diet containing only 2,200 calories. Higher caloric intakes would result in higher intakes of inorganic phosphates, and higher serum phosphate levels, too. And people eating "healthy diets" who use supplements might be getting even higher amounts, since many chalky pill substrates are made mostly of dicalcium phosphate.
How Damaging Is This Added Phosphate?
The Framingham Offspring study found that in normal participants whose serum phosphate levels were in the top quarter of readings for the whole research group at the beginning of the 16 year study there was a 55% higher risk of developing cardiovascular disease at the end of the study . This is a big leap in risk, especially when it is attributed to a factor that is completely ignored by doctors, health authorities, and food companies.
Though we can't be confident in comparing the blood phosphate levels in the 1977 diet study and the Framingham Offspring study, as using different lab techniques will give different reference ranges, it's worth noting that the serum phosphate value representing beginning of the highest quartile in the Framingham Offspring Study--the level at which cardiovascular risk was 55% higher--was only 20% higher than the top of the lowest quartile.
So since we have seen that boosting the phosphate intake of a 2,200 calorie diet can easily achieve an 18% rise in serum phosphate levels, it seems very likely that dietary consumption of phosphates, alone, is enough to boost serum levels into the range that correlates with a higher risk of heart disease.
Is it the Phosphates Causing Heart Disease or Are They A Lifestyle Marker?
Since inorganic phosphate intakes rise dramatically when people eat diets high in fast food and soda, it would be easy to dismiss the link between serum phosphates and heart disease as being due not to the phosphates themselves, but to the unhealthy diet that results in those high serum phosphate levels. In short, to point to serum phosphates as a marker of a diet rich in junk food.
But there is some other research that contradicts this argument. The researchers who published the Framingham Offspring Study cite a study that found that "... higher phosphorus levels increase the propensity of mineral deposition in vascular smooth muscle cells in vitro." That study found that
What this means in plain English is that in a petri dish, cells from heart arteries were fine when exposed to normal levels of phosphates, but when the levels rose to abnormally high levels the artery cells started to act like bone stem cells and fill up with tiny bits of rock. The higher the amount of phosphate they were exposed to, the more rock.
The Framingham researchers also cite a study showing that "higher serum phosphorus levels increase circulating PTH [parathyroid hormone] levels even in healthy individuals," pointing out that "Higher PTH levels may be proinflammatory" as they raise the level of a substance, IL-6, linked to heart disease.
These findings suggest that the problem is that when you eat too much phosphate-containing rock, that rock ends up floating around your bloodstream until it precipitates out in your heart muscle (and other) cells.
Phosphate, Vitamin D, and Niacin
An interesting side note to the issue of high serum phosphate is the finding that rising serum phosphates will lower Vitamin D production as Vitamin D is one of the regulators of blood phosphate levels. (Discussed HERE). If you have abnormally low Vitamin D levels when not supplementing Vitamin D, this could be pointing to the fact that your serum phosphate level is unhealthily high.
In patients with kidney failure, there is some evidence that supplemental niacin lowers the very high serum phosphate levels characteristic of kidney failure, though there is no research to answer the question of whether niacin lowers phosphate levels in people with normal kidneys. But it makes a lot more sense to lower serum phosphate levels by cutting out of your diet as much inorganic phosphate as possible rather than to drive with one foot on your physiological accelerator and one on the brake, which is what you do when you attempt to lower these levels by taking a supplement while consuming the phosphates.
What's Next?
I'll be writing more about the role of inorganic phosphates in our diets and what we can do to achieve normal serum phosphate levels. For now, your homework is to start reading labels for all the foods and supplements you consume, to see how many items you eat each day contain added inorganic phosphate.
Since I started doing this, back when I published my first post about the dangers of high phosphate levels, I've been at first surprised, and then horrified, to see just how much of what I have thought of as "healthy" foods and supplements are full of these dangerous, inorganic phosphate minerals.
Phosphates are compounds that contain phosphorous and oxygen. They are essential to the construction of every cell in our body as phosphates make up the backbone of DNA, They form essential components in cell membranes and are essential to the proper growth of plants. Adenoside Triphosphate (ATP) is the molecule every cell uses used to store energy. Without it, we're dead meat.
Therefore we get a dose of phosphates any time we eat any meat or vegetable. These are "organic phosphates" which are deeply bound into the structure of the foods we eat--so much so that only 40-60% of the phosphate we consume is actually bioavailable. The rest goes through us undigested.
But these organic are not the phosphates that pose a threat to health. The problem phosphates are the "inorganic phosphates"--chunks of phosphate containing rock--that are added to our foods. The are commonly used as preservatives, flavor additives, and to keep cream from separating in dairy products. Phosphoric acid, which converts to phosphate in our bodies, is added to soda to keep brown sodas from turning jet black, which would make them unappealing to most people. Phosphates are also frequently used to provide the chalky white pill material that holds the supplements you buy in pill form.
Unlike the organic phosphates these inorganic phosphates are 100% bioavailable. That means if you eat 500 mg of calcium phosphate, disodium phosphate, or any of the many other inorganic phosphates added to processed foods or supplements, the whole 500 mg will be absorbed. When it is, it will go into your bloodstream where where will raise your serum phosphate level.
It has long been known that consuming inorganic phosphates can be very dangerous for people with severe kidney disease, as failing kidneys can't remove phosphates from teh blood, and these phosphates precipitate out in the kidney, destroying what little function is left. But while doctors may be aware of this, few of them know that consuming inorganic phosphates also poses a major risk to normal people, because it can promote heart disease.
We know from several well-conducted studies that there is a direct link between serum phosphate level and heart disease. As a recently published review article explains, " Higher serum phosphate levels were independently associated with coronary artery calcification, vascular stiffness, left ventricular hypertrophy, and carotid artery disease, even among individuals with normal kidney function and serum phosphate levels within the normal range."
A study that matched CAC scans to serum phosphate levels verified that rising serum phosphate levels correlated directly to rising Agaston scores in a population who had completely normal kidney function.
The most comprehensive study to investigate the impact of phosphates on heart disease was a study of the Framingham Offspring. It looked at serum phosphate levels in a group of over 3,000 normal people and then looked to see which of them had developed heart disease sixteen years later. It found that:
... a higher level of serum phosphorus was associated with an increased CVD [cardiovascular disease] risk in a continuous fashion. ... Individuals in the highest serum phosphorus quartile experienced a multivariable-adjusted 1.55-fold CVD risk ... compared with those in the lowest quartile... Serum calcium was not related to CVD risk.Does Eating Inorganic Phosphates Raise Serum Phosphate Levels?
After reading this, I could not help but wonder if those high serum phosphate levels that caused heart disease were caused by eating diets high in phosphate or whether people destined to get heart disease migh6 have high serum phosphate levels as a side effect of an undiagnosed preexisting health issue.
Could eating a diet high in phosphates be all it took to raise serum phosphate levels? This question was elegantly answered by a study published back in 1977.
In this study subjects who were allowed to eat only the foods supplied by the researchers were, for four weeks, fed a control diet free of any phosphate additives. Then, for the next four weeks, they were fed a diet that contained the identical amount of calories, protein, fat, and carbohydrate as the control diet but this diet was made up of foods containing inorganic phosphate additives, like American cheese, soda, and processed meats.
The report explains, "The average phosphorus content of the daily menu was 979 mg during the control period and 2124 mg during the test period." After a month of eating the foods with the added phosphates, the study participants blood was tested and it was found that they had experienced a dramatic rise in serum phosphates, accompanied by a decrease in serum calcium. The addition of the phosphates to their diets also caused digestive distress to many of the participants--in some cases it persisted throughout the whole study.
When their serum phosphate levels were measured, they were found to have "increased from 3.76 ±0.38 mg/100 ml during the control period to 4.43 ±0.30 mg/ 100 ml [mg/dl] during the high-phosphorus period." This was an 18% rise in serum phosphate level. So yes, upping dietary consumption of inorganic phosphates will raise serum phosphate a lot, even in completely normal people.
And it is also worth noting that the amount of phosphate being consumed by the subjects in this study is likely to be far less than that consumed by the average person today since they were being fed a controlled diet containing only 2,200 calories. Higher caloric intakes would result in higher intakes of inorganic phosphates, and higher serum phosphate levels, too. And people eating "healthy diets" who use supplements might be getting even higher amounts, since many chalky pill substrates are made mostly of dicalcium phosphate.
How Damaging Is This Added Phosphate?
The Framingham Offspring study found that in normal participants whose serum phosphate levels were in the top quarter of readings for the whole research group at the beginning of the 16 year study there was a 55% higher risk of developing cardiovascular disease at the end of the study . This is a big leap in risk, especially when it is attributed to a factor that is completely ignored by doctors, health authorities, and food companies.
Though we can't be confident in comparing the blood phosphate levels in the 1977 diet study and the Framingham Offspring study, as using different lab techniques will give different reference ranges, it's worth noting that the serum phosphate value representing beginning of the highest quartile in the Framingham Offspring Study--the level at which cardiovascular risk was 55% higher--was only 20% higher than the top of the lowest quartile.
So since we have seen that boosting the phosphate intake of a 2,200 calorie diet can easily achieve an 18% rise in serum phosphate levels, it seems very likely that dietary consumption of phosphates, alone, is enough to boost serum levels into the range that correlates with a higher risk of heart disease.
Is it the Phosphates Causing Heart Disease or Are They A Lifestyle Marker?
Since inorganic phosphate intakes rise dramatically when people eat diets high in fast food and soda, it would be easy to dismiss the link between serum phosphates and heart disease as being due not to the phosphates themselves, but to the unhealthy diet that results in those high serum phosphate levels. In short, to point to serum phosphates as a marker of a diet rich in junk food.
But there is some other research that contradicts this argument. The researchers who published the Framingham Offspring Study cite a study that found that "... higher phosphorus levels increase the propensity of mineral deposition in vascular smooth muscle cells in vitro." That study found that
HSMCs -[Aortic Smooth Muscle Cells] cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition.Furthermore, exposure to high levels of phosphates induces a phenotypic transformation of vascular smooth muscle cells into osteoblast-like cells that express biochemical markers characteristic of the cells that turn into bone.
What this means in plain English is that in a petri dish, cells from heart arteries were fine when exposed to normal levels of phosphates, but when the levels rose to abnormally high levels the artery cells started to act like bone stem cells and fill up with tiny bits of rock. The higher the amount of phosphate they were exposed to, the more rock.
The Framingham researchers also cite a study showing that "higher serum phosphorus levels increase circulating PTH [parathyroid hormone] levels even in healthy individuals," pointing out that "Higher PTH levels may be proinflammatory" as they raise the level of a substance, IL-6, linked to heart disease.
These findings suggest that the problem is that when you eat too much phosphate-containing rock, that rock ends up floating around your bloodstream until it precipitates out in your heart muscle (and other) cells.
Phosphate, Vitamin D, and Niacin
An interesting side note to the issue of high serum phosphate is the finding that rising serum phosphates will lower Vitamin D production as Vitamin D is one of the regulators of blood phosphate levels. (Discussed HERE). If you have abnormally low Vitamin D levels when not supplementing Vitamin D, this could be pointing to the fact that your serum phosphate level is unhealthily high.
In patients with kidney failure, there is some evidence that supplemental niacin lowers the very high serum phosphate levels characteristic of kidney failure, though there is no research to answer the question of whether niacin lowers phosphate levels in people with normal kidneys. But it makes a lot more sense to lower serum phosphate levels by cutting out of your diet as much inorganic phosphate as possible rather than to drive with one foot on your physiological accelerator and one on the brake, which is what you do when you attempt to lower these levels by taking a supplement while consuming the phosphates.
What's Next?
I'll be writing more about the role of inorganic phosphates in our diets and what we can do to achieve normal serum phosphate levels. For now, your homework is to start reading labels for all the foods and supplements you consume, to see how many items you eat each day contain added inorganic phosphate.
Since I started doing this, back when I published my first post about the dangers of high phosphate levels, I've been at first surprised, and then horrified, to see just how much of what I have thought of as "healthy" foods and supplements are full of these dangerous, inorganic phosphate minerals.
June 3, 2013
May Diabetes-Related News Snippets
Here are the diabetes news items posted during May, 2013 that may have some lasting value:
6:58 PM, May 04, 2013
Jenny
said...
9:01 AM, May 15, 2013
Jenny
said...
9:12 AM, May 15, 2013
Jenny
said...
9:25 AM, May 15, 2013
Jenny
said...
9:28 AM, May 15, 2013
Jenny
said...
9:34 AM, May 15, 2013
Jenny
said...
9:39 AM, May 15, 2013
Jenny
said...
9:47 AM, May 15, 2013
Jenny
said...
5:31 PM, May 15, 2013
Jenny
said...
1:57 PM, May 24, 2013
Jenny
said...
&nfsp;
Jenny said...
Finally, some research that really does sound like it might go a long way to controlling Type 1 diabetes in a more physiological way.
Science Daily: Injectible Nano Network Controls Blood Sugar in Diabetics for Days at a Time
A subcutaneous network of nanoparticles releases insulin only when blood sugars rise. And yes, the "Diabetics" in this report turn out to be rodents, but I don't see any reason why the concept would work in people too, since it it the chemistry between blood sugar and the network that controls the release of insulin, not anything particularly rodent-specific.
The only challenge that leaps to mind is that humans use a lot more insulin than tiny mice, so could you inject a large enough network to provide the needed insulin?
Let's hope this isn't one of the many promising research avenues that gets bought up and buried by the drug companies who would lose a lot of money if effective treatments for diabetes were to be created.
OTOH, ten days translates into a lot of treatments, and given the obscene amounts that get charged for any truly lifesaving treatment, this one might end up too expensive to be widely deployed.
It's not clear to me from the little I have read about this whether it would be of use to people with Type 2 who are insulin resistant, probably because the amounts of insulin needed with Type 2 can be as much as 10 times higher than those needed to control Type 1. (Or at times even higher.)
Yet another contributing cause to the increase in diabetes: Arsenic compounds fed chickens which turn into pure arsenic when the meat is cooked and eaten.
"Arsenic-based drugs have been used in poultry production for decades. Arsenical drugs are approved to make poultry grow faster and improve the pigmentation of the meat. ...the researchers were able to identify residual roxarsone in the meat they studied; in the meat where roxarsone was detected, levels of inorganic arsenic were four times higher than the levels in USDA Organic chicken (in which roxarsone and other arsenicals are prohibited from use)."
The FDA as is so often the case, doesn't care. You should. Besides causing cancer, arsenic has been shown to raise the incidence of diabetes.
Between the high level of phosphates in most chicken sold today which promote heart disease and the high concentration of antibiotics--and arsenic--in the meat, I think we can safely dismiss the idea that chicken is health food.
Science Daily: Poultry Drug Increases Levels of Toxic Arsenic in Chicken Meat
Doctors may dismiss patient reports that statins damage their ability to think, but the effect is real. A set of studies documents disturbing changes in the neurons following statin use: "unusual swellings within neurons," described as "beads on a string."
This is research on cultured neurons in petri dishes not living people, but it seems significant, given how many people report thinking problems after taking stains.
In the petri dish, removing the statin will reverse the neurological damage. The reports from people are mixed.
Science Daily: Possible Reason for Cholesterol-Drug Side Effects Such as Memory Loss
Measuring the calories in common restaurant meals shows just how out of control portion size has gotten.
"On average, the meals studied contained 1,327 calories, which significantly exceeds the estimated energy needs of an individual adult at a single meal,"
"Nearly three-quarters (73%) of the meals analyzed contained more than half of the FDA's daily energy recommendation of 2,000 calories,"
"Among the meal categories studied, the Italian (1,755 calories), American (1,494 calories) and Chinese (1,474 calories) meals had the highest average calorie levels. Vietnamese meals had the lowest calorie levels as measured by gross energy, with an average of 922 calories. The Japanese meals had the second lowest calories, with an average of 1,027 calories."
Considering that a middle aged woman of normal size can eat no more than 1800 calories a day without gaining weight, it's not surprising how easily we become. That 2,000 calorie a day intake recommendation only works for YOUNG people. With each decade your caloric needs drop, and you would have to exercise for several hours every day to make up for the change age induces.
Science Daily: Individual and Small-Chain Restaurant Meals Exceed Recommended Daily Calorie Needs
Yet another well-documented cause of insulin resistance: The kinds of air pollution given off by motor vehicles. A new study documents its effect on children:
"levels of insulin resistance were greater in children with higher exposure to air pollution. Insulin resistance increased by 17% for every 10.6 µg/m3 (2 standard deviations [SDs] from the mean) increase in ambient nitrogen dioxide (NO2) and 19% for every 6 µg/m3 (2 SDs) increase in particulate matter of up to 10 μm in diameter. Proximity to the nearest major road increased insulin resistance by 7% per 500 metres. All the findings were statistically significant."
Air Pollution Increases Risk of Insulin Resistance in Children
A hormone, aP2, secreted by (mouse) fat cells helps regulate the release of glucose by the liver. Suppressing the secretion of this hormone lowers blood sugar in mice.
Worthy of follow up in people to see if it holds up. Much mouse research doesn't.
Science Daily" Discovery of New Hormone Opens Doors to New Type 2 Diabetes Treatments
Several recent studies have shed light on why it is blood sugar, not a diagnosis of the underlying condition that causes high blood sugar, that damages the body.
Rising blood glucose, it turns out, raises the level of various inflammatory proteins. Inflammation in turn damages the blood vessels including the arteries causing heart disease and those involved in other diabetic complications.
Lowering blood sugar prevents these changes.
Injecting Insulin also decreases inflammation.
University of Buffalo: Study: Insulin fights inflammation and even small amounts of glucose trigger it in Type 1 diabetics Note: the study also documents these effects in people with Type 2 diabetes.
Science Daily: Protecting the Heart Health of Diabetic Patients
A careful study casts doubt on the theory that viral infections are what trigger the development of Type 1 diabetes in children.
Diabetes Daily: No Link Found Between Viral Infection and Rapidly Developing Type 1 Diabetes in Young Children
Marijuana users have better blood sugar control
NHANES data. Is this effect from smoking dope, or do people with normal blood sugar self-select ad habitual users, since they don't get overpowering munchies when they smoke and thus find it more enjoyable?
Yet another large, long population study finds that taking high potency statins raises the risk of developing Type 2 Diabetes.
Conclusion: "Compared with pravastatin, treatment with higher potency statins, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset diabetes."
22% higher risk with Lipitor (atorvastatin) and 18 percent higher with Crestor (rosuvastatin).
In mainstream press coverage, Drug company shills,, a.k.a. well known cardiologists, bend over backward to ignore this latest confirmation of a phenomenon that has been public knowledge for more than a year.
The reason that statins cause diabetes may have to do with the fact that they impair the operation mitochondria--the part of the cell that burns glucose, which is why you are supposed to take Coenzyme Q10 with them
Risk of incident diabetes among patients treated with statins: population based study BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f2610 (Published 23 May 2013)
In press coverage
As I have been writing for years, the condition called "Type 2 Diabetes" is actually many different conditions with different genetic causes. Ethnicity plays a huge role in the kind of diabetes a person might have. The degree to which the problem is lack of insulin secretion or high insulin resistance varies greatly too.
Science Daily: Diabetes Genetic Underpinnings Can Vary Based On Ethnic Background.
This points out just how stupid most rodent research is, as the "Type 2 Diabetes" that lab rodents get is caused by completely different genes than the ones that affect humans. Even in the rare cases when they insert a human gene in a rodent, it is one that causes diabetes in only a small subset of humans.
But mouse research is a lot cheaper than research in humans and there are too many people who have built careers and got inside tracks on grant money using rodents for the situation to change.
Bottom line, remember that eating fat does not cause diabetes in anything but rodents selected as "Models" of diabetes because they get diabetes when they eat fat. Humans get diabetes when they eat more carbs than their genetically weak bodies can tolerate.
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