December 26, 2011
Mitochondrial Diabetes: Another Non-Insulin Resistant Adult Onset Diabetes
I've been reading up on mitochondria this month, in the writings of Nick Lane, Power, Sex, Suicide: Mitochondria and the Meaning of Life, and Oxygen: The Molecule That Made the World. There was a lot of interesting information in both books, but because at times Lane writes in a confused way about the relationship of diabetes and mitochondrial dysfunction, I became curious about what is actually known about mitochondrial failure and diabetes and started reading up on the subject.
It turns out that there is a distinct genetic form of diabetes caused by the A3243G mutation in the mitochondrial DNA-encoded tRNA(Leu,UUR) gene. It causes an adult onset form of diabetes that can be misdiagnosed as either Type 1 or Type 2 depending on how late the onset is. Some people get it in their 20s, while others only develop it in middle age. The average age of onset is 38 years. Whatever the time of onset, 100% of those who have this gene will eventually become diabetic, with a form of diabetes characterized by failure to secrete insulin, rather than insulin resistance.
Like all the genetic forms of diabetes, this is another case where the actual expression of the gene defect can range from very mild to severe. Some people who carry it won't develop diabetes until they are in their 60s, while others may get it in their teens and be misdiagnosed as Type 1 (though the person with it will not show the characteristic antibodies associated with autoimmune Type 1.) The actual percentage of mitochondria carrying the mutation in various tissues will vary from person to person diagnosed with it, and that may have something to do with the severity of the diabetes, as well as whether other damaging effects of the gene are present (discussed below.)
A very severe condition caused by this gene mutation is called MELAS syndrome and reading about its symptoms can be scary, as they include stroke, and a shortened life. But the good news is that now that gene testing is more widely available, scientists are now finding that many people with the same mutation have far less severe manifestations that go undetected until they are gene tested, though these other carriers may have various health problems that seem like the usual wear and tear that are actually byproducts of the gene.
Also, and very interestingly, people with this gene defect, who tend to be thin and at times shorter than their peers, prior to becoming diabetic will have completely normal C-peptide and glucose tolerance tests. However as the gene expresses in their beta cells it apparently causes the mitochondria in the beta cells to fail, leading to the death of the beta cells.
This gene is found in varying frequencies in different ethnic populations. It was found in almost 3% of a Japanese diabetic population, and in about 1% of a group of Dutch people with diabetes. The incidence was lower in those participating in the UKPDS, and in a French population--roughly .5%.
Because mitochondrial genes are passed only from the mother, the family pattern of this genetic form of diabetes appears strictly in the maternal line. Men can get it if their mothers have it, but they cannot pass it on to their children.
This gene defect also appears occasionally spontaneously, so it is possible to have it without a family history but this is very rare.
This gene defect also causes hearing loss in the higher frequency ranges which often becomes evident shortly before the diabetes appears. For that reason this kind of diabetes is also called MIDD (Maternally Inherited Diabetes with Deafness.)
People with this gene may also have a hard-to-detect problem with their heart muscles--asymptomatic cardiomyopathy--which makes it very important that they avoid Avandia and Actos, which have been proven to increase the risk of heart failure in people who take them. The sulfonylurea drugs except gliclazide are also problematic since they also seem to have a negative effect on the heart.
Changes in retinal pigmentation also present in many carriers of the A3243G mutation and they may be more prone than others to develop retinopathy, though it appears that controlling blood sugar will lessen the risk of this happening. Other symptoms which are related to the gene defect can include problems with the digestive tract including diarrhea, obstruction, and severe heartburn.
This gene defect can also cause problems with kidneys that will show up as protein in the urine but are not necessarily linked to high blood sugars, as is typical in diabetes, but are another outcome of the failing mitochondria.
In some people with this gene defect there are other manifestations of mitochondrial failure throughout the body including the inability to tolerate exercise and a frequent migraines. A smaller number have strokes at a young age. This is one reason why you would want to be screened for this gene if you do have the history of diabetes running down the maternal line of your family in conjunction with deafness.
Because mitochondrial failure can cause a rise in lactic acid, people with this form of diabetes should not take metformin as they are at risk for lactic acidosis.
If your family and personal history are suggestive of this kind of diabetes, demand that it be ruled out. It is very possible that your family doctor will NOT have heard of it, so you may have to educate him or her. If you encounter resistance (such as the doctor responding to your showing him one of the articles below by saying, "Where did you earn your M.D.?") find another doctor. This kind of diabetes because it may come with other organ problems requires that you find the support of a very good, up-to-date medical team.
The appropriate treatment for mitochondrial diabetes is insulin, as it brings about the progressive loss of beta cells over time, so it won't be fully controlled by diet. The better you control your blood sugars, the less stress you are putting on those beta cells that remain, so it's likely that very tight control--as close to normal as possible--will have some effect, and of course, it will help prevent the development of the classic diabetic complications.
I have heard from one person diagnosed with MELAS whose diabetes was being controlled with insulin but who was having trouble with her control. She reported that following the "Test test test" strategy this site recommends was helpful for improving her control. You can read about it HERE.
Though I read recommendations online that it is possible to treat milder versions with sulfonylurea drugs, this is probably a bad idea given the recent findings (published after these articles were written) that sulfonylurea drugs can harm the heart.
If you have the symptoms of this form of diabetes you should get your heart checked out by a talented cardiologist--ideally one who practices in a teaching hospital who might have heard of this syndrome, rather than one of the hacks who practices out of a community hospital and prescribes statins to everyone who walks through the door.
As is too often the case with oddball forms of diabetes, most of what you find in scanning the research is diagnostic, rather than information about how to treat the condition. That is probably because it is rare and no one will get rich treating it. If you do have this kind of diabetes it is likely that like everyone else with some form of diabetes your overall health will be better if you keep your blood sugar as close to normal as possible, which even with insulin usually requires keeping a close eye on carbohydrate intake and ratcheting it down until you are avoiding the blood sugar spikes over 140 mg/dl (7.7 mmol/L) that are known to cause the classic diabetic complications.
RESOURCES FOR LEARNING ABOUT MITOCHONDRIAL DIABETES
Mitochondrial Diabetes Molecular Mechanisms and Clinical Presentation.
J. Antonie Maassen et al.Diabetes .53.2007.S103 Diabetes February 2004 vol. 53 no. suppl 1 S103-S109 doi: 10.2337/
Epidemiology and Treatment of Mitochondrial Disorders. Patrick M Chinnery, et al. American Journal of Medical Genetics (Semin. Med. Genet.) 106:94±101 (2001)
Markedly different clinical features in 2 diabetes mellitus patients with extremely high tissue levels of the mitochondrial DNA A3243G mutation. Shinji Harihara. Gerontologia (2008) Volume: 54, Issue: 3, Pages: 168-172
Protean Phenotypic Features of the A3243G Mitochondrial DNA Mutation. Petra Kaufmann et al. Archive of Neurology VOL 66 (NO. 1), JAN 2009
It turns out that there is a distinct genetic form of diabetes caused by the A3243G mutation in the mitochondrial DNA-encoded tRNA(Leu,UUR) gene. It causes an adult onset form of diabetes that can be misdiagnosed as either Type 1 or Type 2 depending on how late the onset is. Some people get it in their 20s, while others only develop it in middle age. The average age of onset is 38 years. Whatever the time of onset, 100% of those who have this gene will eventually become diabetic, with a form of diabetes characterized by failure to secrete insulin, rather than insulin resistance.
Like all the genetic forms of diabetes, this is another case where the actual expression of the gene defect can range from very mild to severe. Some people who carry it won't develop diabetes until they are in their 60s, while others may get it in their teens and be misdiagnosed as Type 1 (though the person with it will not show the characteristic antibodies associated with autoimmune Type 1.) The actual percentage of mitochondria carrying the mutation in various tissues will vary from person to person diagnosed with it, and that may have something to do with the severity of the diabetes, as well as whether other damaging effects of the gene are present (discussed below.)
A very severe condition caused by this gene mutation is called MELAS syndrome and reading about its symptoms can be scary, as they include stroke, and a shortened life. But the good news is that now that gene testing is more widely available, scientists are now finding that many people with the same mutation have far less severe manifestations that go undetected until they are gene tested, though these other carriers may have various health problems that seem like the usual wear and tear that are actually byproducts of the gene.
Also, and very interestingly, people with this gene defect, who tend to be thin and at times shorter than their peers, prior to becoming diabetic will have completely normal C-peptide and glucose tolerance tests. However as the gene expresses in their beta cells it apparently causes the mitochondria in the beta cells to fail, leading to the death of the beta cells.
This gene is found in varying frequencies in different ethnic populations. It was found in almost 3% of a Japanese diabetic population, and in about 1% of a group of Dutch people with diabetes. The incidence was lower in those participating in the UKPDS, and in a French population--roughly .5%.
Because mitochondrial genes are passed only from the mother, the family pattern of this genetic form of diabetes appears strictly in the maternal line. Men can get it if their mothers have it, but they cannot pass it on to their children.
This gene defect also appears occasionally spontaneously, so it is possible to have it without a family history but this is very rare.
This gene defect also causes hearing loss in the higher frequency ranges which often becomes evident shortly before the diabetes appears. For that reason this kind of diabetes is also called MIDD (Maternally Inherited Diabetes with Deafness.)
People with this gene may also have a hard-to-detect problem with their heart muscles--asymptomatic cardiomyopathy--which makes it very important that they avoid Avandia and Actos, which have been proven to increase the risk of heart failure in people who take them. The sulfonylurea drugs except gliclazide are also problematic since they also seem to have a negative effect on the heart.
Changes in retinal pigmentation also present in many carriers of the A3243G mutation and they may be more prone than others to develop retinopathy, though it appears that controlling blood sugar will lessen the risk of this happening. Other symptoms which are related to the gene defect can include problems with the digestive tract including diarrhea, obstruction, and severe heartburn.
This gene defect can also cause problems with kidneys that will show up as protein in the urine but are not necessarily linked to high blood sugars, as is typical in diabetes, but are another outcome of the failing mitochondria.
In some people with this gene defect there are other manifestations of mitochondrial failure throughout the body including the inability to tolerate exercise and a frequent migraines. A smaller number have strokes at a young age. This is one reason why you would want to be screened for this gene if you do have the history of diabetes running down the maternal line of your family in conjunction with deafness.
Because mitochondrial failure can cause a rise in lactic acid, people with this form of diabetes should not take metformin as they are at risk for lactic acidosis.
If your family and personal history are suggestive of this kind of diabetes, demand that it be ruled out. It is very possible that your family doctor will NOT have heard of it, so you may have to educate him or her. If you encounter resistance (such as the doctor responding to your showing him one of the articles below by saying, "Where did you earn your M.D.?") find another doctor. This kind of diabetes because it may come with other organ problems requires that you find the support of a very good, up-to-date medical team.
The appropriate treatment for mitochondrial diabetes is insulin, as it brings about the progressive loss of beta cells over time, so it won't be fully controlled by diet. The better you control your blood sugars, the less stress you are putting on those beta cells that remain, so it's likely that very tight control--as close to normal as possible--will have some effect, and of course, it will help prevent the development of the classic diabetic complications.
I have heard from one person diagnosed with MELAS whose diabetes was being controlled with insulin but who was having trouble with her control. She reported that following the "Test test test" strategy this site recommends was helpful for improving her control. You can read about it HERE.
Though I read recommendations online that it is possible to treat milder versions with sulfonylurea drugs, this is probably a bad idea given the recent findings (published after these articles were written) that sulfonylurea drugs can harm the heart.
If you have the symptoms of this form of diabetes you should get your heart checked out by a talented cardiologist--ideally one who practices in a teaching hospital who might have heard of this syndrome, rather than one of the hacks who practices out of a community hospital and prescribes statins to everyone who walks through the door.
As is too often the case with oddball forms of diabetes, most of what you find in scanning the research is diagnostic, rather than information about how to treat the condition. That is probably because it is rare and no one will get rich treating it. If you do have this kind of diabetes it is likely that like everyone else with some form of diabetes your overall health will be better if you keep your blood sugar as close to normal as possible, which even with insulin usually requires keeping a close eye on carbohydrate intake and ratcheting it down until you are avoiding the blood sugar spikes over 140 mg/dl (7.7 mmol/L) that are known to cause the classic diabetic complications.
RESOURCES FOR LEARNING ABOUT MITOCHONDRIAL DIABETES
Mitochondrial Diabetes Molecular Mechanisms and Clinical Presentation.
J. Antonie Maassen et al.Diabetes .53.2007.S103 Diabetes February 2004 vol. 53 no. suppl 1 S103-S109 doi: 10.2337/
Epidemiology and Treatment of Mitochondrial Disorders. Patrick M Chinnery, et al. American Journal of Medical Genetics (Semin. Med. Genet.) 106:94±101 (2001)
Markedly different clinical features in 2 diabetes mellitus patients with extremely high tissue levels of the mitochondrial DNA A3243G mutation. Shinji Harihara. Gerontologia (2008) Volume: 54, Issue: 3, Pages: 168-172
Protean Phenotypic Features of the A3243G Mitochondrial DNA Mutation. Petra Kaufmann et al. Archive of Neurology VOL 66 (NO. 1), JAN 2009
December 19, 2011
Another Dangrously Misleading Study Promoting High A1cs as Healthy
A presentation given at the recent 44th annual meeting of the American Society of Nephrology claims that patients on dialysis have better outcomes when they have higher A1cs. As reported in Medscape, the chief researcher says, "The range from 6% to 9% seems to be the lower range of risk. There's even an impression that you could say that from 7% to 9% is the lowest risk."
You can read the report of the presentation here. It also got some play in the medical news and newsletters directed to doctors and appears summarized on quite a few diabetes sites. The Medscape article gives the best summary. Signing up is free:
Medscape:Diabetics on Dialysis Do Better With Higher Hemoglobin A1c.
It is all too likely that busy family doctors who encounter this information will add it to the rest of the bad research that has convinced them that it's dangerous for people with Type 2 Diabetes to lower their blood sugars to normal levels. (You can read about how misinterpreted studies have led this toxic recommendation HERE.)
To understand the real meaning of the paper given at American Society of Nephrology you have to know that other research looking into the blood sugars of people on dialysis has found that because of the impact of dialysis on their red blood cells, the A1cs of people on dialysis do not correlate to their blood sugars.
In a published review of the research that discovered the inapplicability of the A1c test to people on dialysis, the author writes
HbA1c Inaccurate in Diabetic Patients on Hemodialysis, Study Says Hogan, Michelle. Nephrology Times: April 2008 - Volume 1 - Issue 4. doi: 10.1097/01.NEP.0000334255.74897.99
The crucial findings of this study were:
Test your blood sugar 1 hour after eating. If your level is under 140 mg/dl (7.7 mmol/L) you are in the range that research suggests will avoid diabetic complications. If you are staying over 140 mg/dl (7.7 mmol/L) for more than an hour or two you are raising your risk of complications. The more time spent over that level, the more likely it is that you are damaging your organs.
The damage doesn't start immediately, and most of us will see occasional readings over that level from time to time that, if they are isolated events, aren't likely to cause damage. But if we are seeing them every day, it's time to take action.
If you are on dialysis, you will want to rely on what you see when you test your blood sugar after meals, not the A1c, to ensure that you aren't worsening whatever other diabetic complications you already have by maintaining damaging high blood sugar levels.
And if you aren't on dialysis and want to keep your nerves, kidneys, eyes and heart healthy, don't let any doctor tell you that it's dangerous to lower your A1c below 6.5%. The evidence suggests that it is not only safe, but very healthy to lower your blood sugar to normal levels, as long as you aren't doing it using Avandia, Actos, Glipizide or Glimiperide all of which have been shown to damage the heart.. The one other "dangerous" way to lower blood sugar is to use insulin in such a way that you balance high blood sugars with hypos. If you are using insulin but never see hypos below 60 mg/dl (3.3 mmol/L) you have nothing to fear.
If you avoid these known dangerous drugs and use carb restriction, metformin, and/or insulin dosed correctly to lower your blood sugar, especially if you start close to diagnosis (or in the pre-diabetic stage) before long term exposure to high blood sugars have damaged your heart, nerves, and blood vessels, your long term outlook should be very good.
And if your doctor disagrees, find a new doctor. Only doctors whose knowledge of diabetes is gleaned only from dumbed down one-paragraph newsletter summaries--or from perky drug company reps who encourage doctors to keep patients at high A1cs because their expensive new drugs only achieve higher than normal A1cs--believe that lowering A1c to normal levels is dangerous.
You can read the report of the presentation here. It also got some play in the medical news and newsletters directed to doctors and appears summarized on quite a few diabetes sites. The Medscape article gives the best summary. Signing up is free:
Medscape:Diabetics on Dialysis Do Better With Higher Hemoglobin A1c.
It is all too likely that busy family doctors who encounter this information will add it to the rest of the bad research that has convinced them that it's dangerous for people with Type 2 Diabetes to lower their blood sugars to normal levels. (You can read about how misinterpreted studies have led this toxic recommendation HERE.)
To understand the real meaning of the paper given at American Society of Nephrology you have to know that other research looking into the blood sugars of people on dialysis has found that because of the impact of dialysis on their red blood cells, the A1cs of people on dialysis do not correlate to their blood sugars.
In a published review of the research that discovered the inapplicability of the A1c test to people on dialysis, the author writes
We expected maybe the hemoglobin A1c would be slightly impacted by the shortened red cell survival when we went into the study, but the results were shocking to us in that the hemoglobin A1c levels were significantly lower to where they would affect patient care and outcomes.You can read this report here:
HbA1c Inaccurate in Diabetic Patients on Hemodialysis, Study Says Hogan, Michelle. Nephrology Times: April 2008 - Volume 1 - Issue 4. doi: 10.1097/01.NEP.0000334255.74897.99
The crucial findings of this study were:
Compared with patients who did not have kidney disease, patients with end-stage renal disease had higher mean serum glucose concentrations-172 mg/dL vs 146 mg/dL-and higher percent glycated albumin-18.7% vs 15.3%-but lower hemoglobin A1c-6.8% vs 7.3%.There is another test that gives a better idea of blood sugar control over a longer time period, but it isn't available in the U.S.. What is available is testing with your blood sugar meter--which is more accurate in predicting health outcomes than the A1c ever was.
For a glucose level of 150 mg/dL, for example, hemoglobin A1c was about 6.5% in the dialysis group but 7.5% in the normal renal function group.
Test your blood sugar 1 hour after eating. If your level is under 140 mg/dl (7.7 mmol/L) you are in the range that research suggests will avoid diabetic complications. If you are staying over 140 mg/dl (7.7 mmol/L) for more than an hour or two you are raising your risk of complications. The more time spent over that level, the more likely it is that you are damaging your organs.
The damage doesn't start immediately, and most of us will see occasional readings over that level from time to time that, if they are isolated events, aren't likely to cause damage. But if we are seeing them every day, it's time to take action.
If you are on dialysis, you will want to rely on what you see when you test your blood sugar after meals, not the A1c, to ensure that you aren't worsening whatever other diabetic complications you already have by maintaining damaging high blood sugar levels.
And if you aren't on dialysis and want to keep your nerves, kidneys, eyes and heart healthy, don't let any doctor tell you that it's dangerous to lower your A1c below 6.5%. The evidence suggests that it is not only safe, but very healthy to lower your blood sugar to normal levels, as long as you aren't doing it using Avandia, Actos, Glipizide or Glimiperide all of which have been shown to damage the heart.. The one other "dangerous" way to lower blood sugar is to use insulin in such a way that you balance high blood sugars with hypos. If you are using insulin but never see hypos below 60 mg/dl (3.3 mmol/L) you have nothing to fear.
If you avoid these known dangerous drugs and use carb restriction, metformin, and/or insulin dosed correctly to lower your blood sugar, especially if you start close to diagnosis (or in the pre-diabetic stage) before long term exposure to high blood sugars have damaged your heart, nerves, and blood vessels, your long term outlook should be very good.
And if your doctor disagrees, find a new doctor. Only doctors whose knowledge of diabetes is gleaned only from dumbed down one-paragraph newsletter summaries--or from perky drug company reps who encourage doctors to keep patients at high A1cs because their expensive new drugs only achieve higher than normal A1cs--believe that lowering A1c to normal levels is dangerous.
November 30, 2011
For Colorectal Cancer It's the Blood Sugar NOT The Insulin Level That Counts
A recently published study based on data from the Womans Health Initiative (WHI) sheds light on a question many of us have wondered about: Is the higher incidence of cancer among people with Type 2 caused by higher insulin levels (or, perhaps injected insulin) or something else?
The study was conducted by a team at The Albert Einstein College of Medicine, which some of you may remember is where Dr. Bernstein earned his M.D.. It has through the years done several low carb studies, too.
The study is summarized here:
Science Daily: High Blood Sugar Levels in Older Women Linked to Colorectal Cancer
The actual abstract is found here:
A longitudinal study of serum insulin and glucose levels in relation to colorectal cancer risk among postmenopausal women. G C Kabat et al. British Journal of Cancer , (29 November 2011) | doi:10.1038/bjc.2011.512
From the abstract we learn that in a group of 4902 middle aged women who were tracked for 12 years, about 1.6 percent developed colorectal cancer. They had had their fasting blood sugar and fasting insulin measured at the beginning of the study and occasionally through the study. This study found that women whose fasting blood sugar was over 99.5 mg/dl (5.53 mmol/L) at the beginning of the study had a greater risk of developing colorectal cancer than those with blood sugars under 89.5 mg/dl (4.98 mmol/L). The relationship held true for subsequent blood tests too.
However--and this is what is interesting about this study--there was no relationship between these women's fasting insulin levels or the calculated HOMA values (which are believed to measure insulin resistance) and their risk of getting this cancer.
So this data would suggest that it is the high blood sugars, not the high insulin which promotes the cancer.
Before you panic because your fasting blood sugar is over 99.5 mg/dl (as is the case with many of us thanks to dawn phenomenon) remind yourself of this: from what we can see in other contexts, it isn't actually mildly elevated fasting blood sugars that damage our bodies. We see the correlation between fasting sugars and complications in studies because in people eating high carbohydrate diets, mildly elevated fasting blood sugars almost always go hand in hand with significantly elevated post meal sugars. Especially in women, who may be diabetic by glucose tolerance test for up to a decade before they would be diagnosed using a fasting glucose test. (You can see the data backing this up HERE.)
So a woman with a fasting sugar of 105 mg/dl, for example, when she eats her morning bagel with jelly, along with a sweetened latte, may easily reach a blood sugar that approaches 200 mg/dl even if it resolves fairly quickly due to a near-healthy second phase insulin release. But if diabetic you should wake up with a blood sugar of 105 mg/dl and eat an egg and bacon for your breakfast with no carbs, you may easily end up with a blood sugar of 95 an hour later, which suggests you would have a similar health outcome to a completely non-diabetic woman with a fasting blood sugar of 89 mg/dl who ends up at 95 mg/dl an hour after eating her breakfast.
It's also worth noting that the statistical measure the study calculated was "risk" not incidence--and that risk is a statistical artifact that magnifies numbers to provide a more dramatic impact. The actual increase in incididence due to elevated blood sugar was likely around 5 cases per thousand or .5%.
But on the positive side, the fact that even after using magifying statistical techniques like "risk" the researchers couldn't find the expected connection between fasting insulin levels, HOMA, and cancer gives us one more, intriguing, piece of data to answer the quesion, "Do people with diabetes get cancer because of high insulin levels (injected or natural) or because of high blood sugars?" Here at least, it looks like the answer is, as is the case with all the other diabetic complications, "It's the blood sugars, stupid!"
This is very good news because our insulin levels are very hard to control and insulin resistance may be genetic and not something we can lower. Even many devout low carbers with Type 2 continue to be insulin resistant no matter what they weigh (based on how much insulin they have to inject to lower their blood sugars.) But insulin resistant or not, we can control our blood sugars--often most effectively with insulin--and if the conclusion of this study is reinforced by findings in other studies, we may be able to relax about the potential impact on cancer of our injecting insulin to control those blood sugars.
One last note: If you have had years of exposure to higher than normal blood sugars, you might be interested in knowing that Metformin has been shown to suppress the growth of existing early colorectal growths in people without diabetes. Read about that HERE.
Though researchers often state that metformin inhibits cancer due to its effect on lowering insulin, this is just a guess. The belief that it is high insulin levels that cause a greater incidence of cancer among people with diabetes is far from proven and that theory is exactly the belief this study debunks.
In fact, there is evidence emerging that metformin's anti-cancer properties are independent of its effect on insulin and have to do with its ability to suppress TORC1, a cell growth factor. (For example, see THIS STUDY.)
NOTE: Since posting this I have reviewed the full text of the study and see nothing to change the conclusions discussed here. It looks very well conducted, involved people from various well-respected public health departments in universities and medical schools, and gives no hint of corporate meddling.
The study was conducted by a team at The Albert Einstein College of Medicine, which some of you may remember is where Dr. Bernstein earned his M.D.. It has through the years done several low carb studies, too.
The study is summarized here:
Science Daily: High Blood Sugar Levels in Older Women Linked to Colorectal Cancer
The actual abstract is found here:
A longitudinal study of serum insulin and glucose levels in relation to colorectal cancer risk among postmenopausal women. G C Kabat et al. British Journal of Cancer , (29 November 2011) | doi:10.1038/bjc.2011.512
From the abstract we learn that in a group of 4902 middle aged women who were tracked for 12 years, about 1.6 percent developed colorectal cancer. They had had their fasting blood sugar and fasting insulin measured at the beginning of the study and occasionally through the study. This study found that women whose fasting blood sugar was over 99.5 mg/dl (5.53 mmol/L) at the beginning of the study had a greater risk of developing colorectal cancer than those with blood sugars under 89.5 mg/dl (4.98 mmol/L). The relationship held true for subsequent blood tests too.
However--and this is what is interesting about this study--there was no relationship between these women's fasting insulin levels or the calculated HOMA values (which are believed to measure insulin resistance) and their risk of getting this cancer.
So this data would suggest that it is the high blood sugars, not the high insulin which promotes the cancer.
Before you panic because your fasting blood sugar is over 99.5 mg/dl (as is the case with many of us thanks to dawn phenomenon) remind yourself of this: from what we can see in other contexts, it isn't actually mildly elevated fasting blood sugars that damage our bodies. We see the correlation between fasting sugars and complications in studies because in people eating high carbohydrate diets, mildly elevated fasting blood sugars almost always go hand in hand with significantly elevated post meal sugars. Especially in women, who may be diabetic by glucose tolerance test for up to a decade before they would be diagnosed using a fasting glucose test. (You can see the data backing this up HERE.)
So a woman with a fasting sugar of 105 mg/dl, for example, when she eats her morning bagel with jelly, along with a sweetened latte, may easily reach a blood sugar that approaches 200 mg/dl even if it resolves fairly quickly due to a near-healthy second phase insulin release. But if diabetic you should wake up with a blood sugar of 105 mg/dl and eat an egg and bacon for your breakfast with no carbs, you may easily end up with a blood sugar of 95 an hour later, which suggests you would have a similar health outcome to a completely non-diabetic woman with a fasting blood sugar of 89 mg/dl who ends up at 95 mg/dl an hour after eating her breakfast.
It's also worth noting that the statistical measure the study calculated was "risk" not incidence--and that risk is a statistical artifact that magnifies numbers to provide a more dramatic impact. The actual increase in incididence due to elevated blood sugar was likely around 5 cases per thousand or .5%.
But on the positive side, the fact that even after using magifying statistical techniques like "risk" the researchers couldn't find the expected connection between fasting insulin levels, HOMA, and cancer gives us one more, intriguing, piece of data to answer the quesion, "Do people with diabetes get cancer because of high insulin levels (injected or natural) or because of high blood sugars?" Here at least, it looks like the answer is, as is the case with all the other diabetic complications, "It's the blood sugars, stupid!"
This is very good news because our insulin levels are very hard to control and insulin resistance may be genetic and not something we can lower. Even many devout low carbers with Type 2 continue to be insulin resistant no matter what they weigh (based on how much insulin they have to inject to lower their blood sugars.) But insulin resistant or not, we can control our blood sugars--often most effectively with insulin--and if the conclusion of this study is reinforced by findings in other studies, we may be able to relax about the potential impact on cancer of our injecting insulin to control those blood sugars.
One last note: If you have had years of exposure to higher than normal blood sugars, you might be interested in knowing that Metformin has been shown to suppress the growth of existing early colorectal growths in people without diabetes. Read about that HERE.
Though researchers often state that metformin inhibits cancer due to its effect on lowering insulin, this is just a guess. The belief that it is high insulin levels that cause a greater incidence of cancer among people with diabetes is far from proven and that theory is exactly the belief this study debunks.
In fact, there is evidence emerging that metformin's anti-cancer properties are independent of its effect on insulin and have to do with its ability to suppress TORC1, a cell growth factor. (For example, see THIS STUDY.)
NOTE: Since posting this I have reviewed the full text of the study and see nothing to change the conclusions discussed here. It looks very well conducted, involved people from various well-respected public health departments in universities and medical schools, and gives no hint of corporate meddling.
November 12, 2011
Another Book?
Now that I've discharged my obligations under my contract with the publisher of my novels, I'm considering what to do next. And that is leading me to ask what I could do that would be of use to the people who visit http://Bloodsugar101.com and this blog.
Publishing the book version of the site has taught me that most people still find books a better way to study a complex topic, even when the information in the book is also available on a web site.
This has been a pleasant surprise, as has been the steady stream of fan mail that the book generates. There's no question that people who read the book learn far more than people who visit the site, if for no other reason than that most people who visit the site only read a couple pages before leaving.
So that raises the question: Should I write another book? And if I do, what should be its subject?
I have some ideas of my own, but before I plunge in I'd love to hear some feedback from you about what topics you would like to learn more about. I'd also like to know, iIf you read my book, Blood Sugar 101, if you thought there was something important that was left out.
Keep in mind, of course, that there are many topics I'd love to be able to write about that are too poorly researched to justify a book. For example, I have spent quite a lot of time looking into the physiology of weight loss, but the more research I read, the less conviction I have that any of it can be trusted. The quality is just abysmal and unlike the publications about diabetes, my many hours of study did not turn up any overlooked gems.
On the other hand, very little has come up that is new since I wrote Blood Sugar 101. In fact, it is rather depressing just how little that would be of any use to someone trying to preserve their health.
But though I might feel that way, life has taught me that one problem with making yourself into an "expert" in some topic area is that the things that bore me after a decade of daily attention to the topic may be exciting to people who haven't soaked their head in this stuff for years.
So I welcome your feedback. What kind of book--if any--do you think would be most useful to a reader who has already read Blood Sugar 101? Click on the comment link below and share your thoughts with me. The only thing I will ask is that you keep your comments on the topic I've sketched out here.
If you want to ask questions or debate other diabetes-related issues, there's a nice community growing on the Blood Sugar 101 Facebook page, where you are welcome to post your thoughts on topics other than the subject of this post.
Publishing the book version of the site has taught me that most people still find books a better way to study a complex topic, even when the information in the book is also available on a web site.
This has been a pleasant surprise, as has been the steady stream of fan mail that the book generates. There's no question that people who read the book learn far more than people who visit the site, if for no other reason than that most people who visit the site only read a couple pages before leaving.
So that raises the question: Should I write another book? And if I do, what should be its subject?
I have some ideas of my own, but before I plunge in I'd love to hear some feedback from you about what topics you would like to learn more about. I'd also like to know, iIf you read my book, Blood Sugar 101, if you thought there was something important that was left out.
Keep in mind, of course, that there are many topics I'd love to be able to write about that are too poorly researched to justify a book. For example, I have spent quite a lot of time looking into the physiology of weight loss, but the more research I read, the less conviction I have that any of it can be trusted. The quality is just abysmal and unlike the publications about diabetes, my many hours of study did not turn up any overlooked gems.
On the other hand, very little has come up that is new since I wrote Blood Sugar 101. In fact, it is rather depressing just how little that would be of any use to someone trying to preserve their health.
But though I might feel that way, life has taught me that one problem with making yourself into an "expert" in some topic area is that the things that bore me after a decade of daily attention to the topic may be exciting to people who haven't soaked their head in this stuff for years.
So I welcome your feedback. What kind of book--if any--do you think would be most useful to a reader who has already read Blood Sugar 101? Click on the comment link below and share your thoughts with me. The only thing I will ask is that you keep your comments on the topic I've sketched out here.
If you want to ask questions or debate other diabetes-related issues, there's a nice community growing on the Blood Sugar 101 Facebook page, where you are welcome to post your thoughts on topics other than the subject of this post.
October 5, 2011
Normal Blood Sugars in Pregnancy
I have until now avoided discussing the issue of what normal blood sugars should be in pregnancy because it looked like gynecologists were being more aggressive with blood sugar control during pregnancy then other doctors.
Blood sugar control is particularly important in pregnancy because a fetus that is exposed to continually high blood sugars will experience significant changes in the way that its genes express which will affect its blood sugar metabolism for the rest of its life.
High blood sugar will also make babies very large, which poses problems when it is time for delivery, some life-threatening.
Blood sugars are lower in pregnant women because there is a higher blood volume during pregnancy, but it is starting to look like the targets gynecologists have been recommending, which would have been excellent for non-diabetic women are considerably higher than normal.
This was made clear by a new meta-study that analyzed a series of studies of the blood sugars of a wide range of normal pregnant women using Continuous Glucose Monitoring, home testing, and hospital lab results. It makes it clear that the current targets for pregnancy are probably too high.
Here is the full text version of the meta-study:
Patterns of Glycemia in Normal Pregnancy: Should the current therapeutic targets be challenged? Teri L. Hernandez, et al. Diabetes Care July 2011 vol. 34 no. 7 1660-1668.
It concludes that the following appear to be truly normal blood sugars for pregnant women:
AVERAGE BLOOD SUGARS IN NORMAL PREGNANT WOMEN
Fasting: 70.9 ± 7.8 mg/dl (3.94 mmol/L ± .43)
One Hour Post Meal: 108.9 ± 12.9 mg/dl (6.05 ± .72 mmol/L)
Two Hours Post Meal: 99.3 ±10.2 mg/dl (5.52 ± .57 mmol/L )
A commentary published in this month's Diabetes Care gives more insight into the importance of this study and why doctors should aggressively lower blood sugars in pregnancy. You can read it HERE. The Full text version is free.
The commentary suggests that pregnant women should strive for blood sugars that don't exceed the first standard deviation of normal (that's the average with the number following the "±" added to it. Doing that gives us targets that should not exceed
RECOMMENDED MAXIMUM BLOOD SUGARS FOR PREGNANT WOMEN WITH DIABETES
Fasting: 79 mg/dl (4.4 mmol/L)
One Hour After Meals: 122 mg/dl (6.8 mmol/L)
Two Hours After Meals: 110 m/gdl (6.1 mmol/L)
The challenge during pregnancy, of course, is to lower blood sugar without going too low because hypos can also cause problems for the fetus. In addition, the solution that works so well for non-pregnant people--cutting way back on carbs--raises issues.
Very low carb diets raise the concentration of ketones in the blood. This isn't a problem when we aren't pregnant--most of our organs can run quite happily burning ketones. But because ketones are usually produced when humans are starving, it is very possible that fetuses produced when the mother is in a ketogenic state may end up with environmentally-produced permanent changes to their genes (epigenetic changes, to use a technical term) that will predispose them to gaining weight once they are born, because ketones may signal the forming baby that they are being born into an environment of scarcity.
The fact that ketogenic diets downregulate T3 and slow the thyroid in non-pregnant people raises the question about whether a ketogenic diet might also have a negative effect on the baby's developing thyroid.
So it's generally considered to be best for pregnant women to lower their blood sugar as much as possible by cutting back on carbohydrates but to keep their carbs over the threshold (anywhere from 60-100 grams a day) where glycogen is depleted and the concentration of ketones in the blood and urine rises.
You can usually detect your own ketogenic threshold easily: it is the carbohydrate intake level at which, after eating at that level for three days, you suddenly lose anywhere from 3 to 8 lbs (depending on your size.) Raising carbs will immediately restore those quickly lost pounds because they are not fat (or growing baby) but the glycogen stored in your liver and muscles which gets burned away when your carbohydrate level is too low to replenish it.
If you eat only enough carbohydrates to keep your glycogen replenished, you won't have to worry that ketones will give your fetus the message that it's being born into an environment where starvation is occurring and shift its genes into a state where they optimize fat storage.
If you can't lower your blood sugar during pregnancy with diet alone, insulin is a safe medication for pregnant women and most doctors provide pregnant women with diabetes much better education in how to use insulin than family doctors do to their non-pregnant peers.
If you are reading this because you are pregnant and have just discovered you have gestational diabetes though you were not diabetic before your pregnancy, here's one last important fact to keep in mind: abnormal blood sugars in pregnancy almost always point to the pre-existence of abnormal sugars in the non-pregnant state that were missed by your doctor because the tests doctors use to screen for diabetes do a woefully bad job of diagnosing it until you have suffered years of high blood sugars that may irreversibly damage your organs.
Once you deliver your baby, don't rely on doctors to tell you if your blood sugar is normal. Test your blood sugar after meals every so often with a meter to make sure that you are not going over the 140 mg/dl (7.7 mmol/L) level at one hour that is truly normal in the non-pregnant state and that you are under 120 mg/dl (ideally far under) at two hours. If you are going over these levels, cut back on your carbohydrates and if that doesn't help, find a doctor willing to work with you to use safe drugs like metformin that can keep your sugars in the normal range for life.
Don't rely on the A1c test, as most doctors now do. It has been shown to be a poor guide to the high post-meal sugars that characterize the very early stages of Type 2 diabetes and which cause heart disease and early diabetic complications.
Blood sugar control is particularly important in pregnancy because a fetus that is exposed to continually high blood sugars will experience significant changes in the way that its genes express which will affect its blood sugar metabolism for the rest of its life.
High blood sugar will also make babies very large, which poses problems when it is time for delivery, some life-threatening.
Blood sugars are lower in pregnant women because there is a higher blood volume during pregnancy, but it is starting to look like the targets gynecologists have been recommending, which would have been excellent for non-diabetic women are considerably higher than normal.
This was made clear by a new meta-study that analyzed a series of studies of the blood sugars of a wide range of normal pregnant women using Continuous Glucose Monitoring, home testing, and hospital lab results. It makes it clear that the current targets for pregnancy are probably too high.
Here is the full text version of the meta-study:
Patterns of Glycemia in Normal Pregnancy: Should the current therapeutic targets be challenged? Teri L. Hernandez, et al. Diabetes Care July 2011 vol. 34 no. 7 1660-1668.
It concludes that the following appear to be truly normal blood sugars for pregnant women:
AVERAGE BLOOD SUGARS IN NORMAL PREGNANT WOMEN
Fasting: 70.9 ± 7.8 mg/dl (3.94 mmol/L ± .43)
One Hour Post Meal: 108.9 ± 12.9 mg/dl (6.05 ± .72 mmol/L)
Two Hours Post Meal: 99.3 ±10.2 mg/dl (5.52 ± .57 mmol/L )
A commentary published in this month's Diabetes Care gives more insight into the importance of this study and why doctors should aggressively lower blood sugars in pregnancy. You can read it HERE. The Full text version is free.
The commentary suggests that pregnant women should strive for blood sugars that don't exceed the first standard deviation of normal (that's the average with the number following the "±" added to it. Doing that gives us targets that should not exceed
RECOMMENDED MAXIMUM BLOOD SUGARS FOR PREGNANT WOMEN WITH DIABETES
Fasting: 79 mg/dl (4.4 mmol/L)
One Hour After Meals: 122 mg/dl (6.8 mmol/L)
Two Hours After Meals: 110 m/gdl (6.1 mmol/L)
The challenge during pregnancy, of course, is to lower blood sugar without going too low because hypos can also cause problems for the fetus. In addition, the solution that works so well for non-pregnant people--cutting way back on carbs--raises issues.
Very low carb diets raise the concentration of ketones in the blood. This isn't a problem when we aren't pregnant--most of our organs can run quite happily burning ketones. But because ketones are usually produced when humans are starving, it is very possible that fetuses produced when the mother is in a ketogenic state may end up with environmentally-produced permanent changes to their genes (epigenetic changes, to use a technical term) that will predispose them to gaining weight once they are born, because ketones may signal the forming baby that they are being born into an environment of scarcity.
The fact that ketogenic diets downregulate T3 and slow the thyroid in non-pregnant people raises the question about whether a ketogenic diet might also have a negative effect on the baby's developing thyroid.
So it's generally considered to be best for pregnant women to lower their blood sugar as much as possible by cutting back on carbohydrates but to keep their carbs over the threshold (anywhere from 60-100 grams a day) where glycogen is depleted and the concentration of ketones in the blood and urine rises.
You can usually detect your own ketogenic threshold easily: it is the carbohydrate intake level at which, after eating at that level for three days, you suddenly lose anywhere from 3 to 8 lbs (depending on your size.) Raising carbs will immediately restore those quickly lost pounds because they are not fat (or growing baby) but the glycogen stored in your liver and muscles which gets burned away when your carbohydrate level is too low to replenish it.
If you eat only enough carbohydrates to keep your glycogen replenished, you won't have to worry that ketones will give your fetus the message that it's being born into an environment where starvation is occurring and shift its genes into a state where they optimize fat storage.
If you can't lower your blood sugar during pregnancy with diet alone, insulin is a safe medication for pregnant women and most doctors provide pregnant women with diabetes much better education in how to use insulin than family doctors do to their non-pregnant peers.
If you are reading this because you are pregnant and have just discovered you have gestational diabetes though you were not diabetic before your pregnancy, here's one last important fact to keep in mind: abnormal blood sugars in pregnancy almost always point to the pre-existence of abnormal sugars in the non-pregnant state that were missed by your doctor because the tests doctors use to screen for diabetes do a woefully bad job of diagnosing it until you have suffered years of high blood sugars that may irreversibly damage your organs.
Once you deliver your baby, don't rely on doctors to tell you if your blood sugar is normal. Test your blood sugar after meals every so often with a meter to make sure that you are not going over the 140 mg/dl (7.7 mmol/L) level at one hour that is truly normal in the non-pregnant state and that you are under 120 mg/dl (ideally far under) at two hours. If you are going over these levels, cut back on your carbohydrates and if that doesn't help, find a doctor willing to work with you to use safe drugs like metformin that can keep your sugars in the normal range for life.
Don't rely on the A1c test, as most doctors now do. It has been shown to be a poor guide to the high post-meal sugars that characterize the very early stages of Type 2 diabetes and which cause heart disease and early diabetic complications.
October 2, 2011
Flawed Logic: Eating "Eggs" or "Meat" is Associated with but Does Not CAUSE Cancer
Today the morning news carried this headline: Eggs may Increase Risk Of Lethal Prostate Cancer In Healthy Men. The article starts out by saying that "we already know red and processed meat may increase risk of advanced prostate cancer" and then claims that eggs are just as dangerous.
The actual study is found here:
Egg, red meat, and poultry intake and risk of lethal prostate cancer in the prostate specific antigen-era: incidence and survival. Erin Richman et al., Cancer Prev Res. 2011 Sep 19. [Epub ahead of print]doi: 10.1158/1940-6207.CAPR-11-0354
The study draws its conclusions by looking at 27,607 men followed between 1994-2008. Of these 199 died of prostate cancer. So the researchers analyzed their food consumption and concluded that "men who consumed 2.5 or more eggs per week had an 81% increased risk of lethal prostate cancer compared to men who consumed less than 0.5 eggs per week (HR: 1.81; 95% confidence interval (CI): 1.13, 2.89; p-trend: 0.01)."
Now the first question you have to ask is this. With 27,607 men involved, how did they know how many eggs they ate? And the answer of course is the infamous standard nutritional questionnaire, beloved by nutrition researchers, which is nearly useless for understanding what people really eat.
I've discussed what's wrong with this questionnaire HERE and suggest you read the section headed "1.Based on Inaccurate Questionnaire Data." to better understand the problem here.
In brief, this questionnaire determines how many eggs you've eaten by asking multiple choice questions like "How many eggs did you eat during the past month." The answers you can choose from are very broad along the lines of . "Never, 1-5 times, 6-20 times, more than 21 times."
The chances that the average middle aged man can accurately remember how many eggs he ate during the past month are low, and even if he did, there's a big difference between 6 and 20 eggs which the questionnaire makes it impossible to discover.
But the real problem here is that the way the questions are phrased. In these questionnaires, the subject is asked how many time a day they eat potatoes or bread, but the multiple choice answers assume at least 2 servings a day for each so you would have to say you ate potatoes or bread five or six times a day for the questionnaire software to notice anything odd about your potato or bread intake at all.
But what the questionnaire doesn't ask this: "Did you eat your eggs with toast? "Did you eat your eggs with pancakes and syrup?" "Did you eat your eggs with biscuits?" Or even, "Did you eat your eggs with a large latte?" In fact, it probably doesn't ask about large lattes at all--because one problem with the questionnaire is that the foods it asks about are generic.
Add to this the problem that when a nutritionist thinks of a serving of a food like pancakes, they are thinking of nutritional database values, so the questionnaire does not account for the fact that "one serving" of "pancakes" or "potatoes" at most restaurants today are actually the size of four servings as defined in nutritional databases. So the person reporting that they drank a Latte can only report that they drank "Coffee with sugar," which the software treats as having 8 grams of carbohydrate, rather than as the 66 gram montstrosity the subject drank at Starbucks.
So of course, you can now see where this is going. Men who eat eggs are not eating an egg or two in isolation. Come on guys. I've seen you eat breakfast. And what I've seen is that when a man who is not on a strict diet eats breakfast (and that's 98% of most men) They're eating 2 eggs, ham, bacon or sausage, a big serving of home fries and two slices of toast. If they eat their "egg" at McDonalds or some other fast food outlet, they're very likely having it with a large Coke, or a frappaccino with 88 grams of sugar. They may be having it with a 68 gram Bear Claw from Panera Bread. In short, the egg, which the subject remembers ("I had eggs at Macdonalds) is a marker for a bunch of starch and sugar at goes unnoticed.
We KNOW for a fact that tumors feast on glucose and that high blood sugar promotes the growth of cancers. In constrast, we know of no reason why eating an egg should damage health. Eating dggs, contrary to popular belief, makes no significant difference in people's cholesterol level (not that cholesterol causes cancer, either). Eggs are almost all protein and we know of no connection between eating normal dietary levels of protein. So the real conclusion that should sum up this study should have been this:
In the unlikely case that these questionnaires accurately represent what the men who died of prostate cancer ate, and that the memory of consuming eggs actually correlates with an increase in fatal cancers, this association could be explained by the fact that subjects who consumed eggs ate them in meals containing large amounts of dietary carbohydrate and damaged fats, a circumstance our nutritional questionnaire is incapable of detecting. Remember, too, that association is not causation, and ignore this study until someone comes up with one that uses a better study design.
The actual study is found here:
Egg, red meat, and poultry intake and risk of lethal prostate cancer in the prostate specific antigen-era: incidence and survival. Erin Richman et al., Cancer Prev Res. 2011 Sep 19. [Epub ahead of print]doi: 10.1158/1940-6207.CAPR-11-0354
The study draws its conclusions by looking at 27,607 men followed between 1994-2008. Of these 199 died of prostate cancer. So the researchers analyzed their food consumption and concluded that "men who consumed 2.5 or more eggs per week had an 81% increased risk of lethal prostate cancer compared to men who consumed less than 0.5 eggs per week (HR: 1.81; 95% confidence interval (CI): 1.13, 2.89; p-trend: 0.01)."
Now the first question you have to ask is this. With 27,607 men involved, how did they know how many eggs they ate? And the answer of course is the infamous standard nutritional questionnaire, beloved by nutrition researchers, which is nearly useless for understanding what people really eat.
I've discussed what's wrong with this questionnaire HERE and suggest you read the section headed "1.Based on Inaccurate Questionnaire Data." to better understand the problem here.
In brief, this questionnaire determines how many eggs you've eaten by asking multiple choice questions like "How many eggs did you eat during the past month." The answers you can choose from are very broad along the lines of . "Never, 1-5 times, 6-20 times, more than 21 times."
The chances that the average middle aged man can accurately remember how many eggs he ate during the past month are low, and even if he did, there's a big difference between 6 and 20 eggs which the questionnaire makes it impossible to discover.
But the real problem here is that the way the questions are phrased. In these questionnaires, the subject is asked how many time a day they eat potatoes or bread, but the multiple choice answers assume at least 2 servings a day for each so you would have to say you ate potatoes or bread five or six times a day for the questionnaire software to notice anything odd about your potato or bread intake at all.
But what the questionnaire doesn't ask this: "Did you eat your eggs with toast? "Did you eat your eggs with pancakes and syrup?" "Did you eat your eggs with biscuits?" Or even, "Did you eat your eggs with a large latte?" In fact, it probably doesn't ask about large lattes at all--because one problem with the questionnaire is that the foods it asks about are generic.
Add to this the problem that when a nutritionist thinks of a serving of a food like pancakes, they are thinking of nutritional database values, so the questionnaire does not account for the fact that "one serving" of "pancakes" or "potatoes" at most restaurants today are actually the size of four servings as defined in nutritional databases. So the person reporting that they drank a Latte can only report that they drank "Coffee with sugar," which the software treats as having 8 grams of carbohydrate, rather than as the 66 gram montstrosity the subject drank at Starbucks.
So of course, you can now see where this is going. Men who eat eggs are not eating an egg or two in isolation. Come on guys. I've seen you eat breakfast. And what I've seen is that when a man who is not on a strict diet eats breakfast (and that's 98% of most men) They're eating 2 eggs, ham, bacon or sausage, a big serving of home fries and two slices of toast. If they eat their "egg" at McDonalds or some other fast food outlet, they're very likely having it with a large Coke, or a frappaccino with 88 grams of sugar. They may be having it with a 68 gram Bear Claw from Panera Bread. In short, the egg, which the subject remembers ("I had eggs at Macdonalds) is a marker for a bunch of starch and sugar at goes unnoticed.
We KNOW for a fact that tumors feast on glucose and that high blood sugar promotes the growth of cancers. In constrast, we know of no reason why eating an egg should damage health. Eating dggs, contrary to popular belief, makes no significant difference in people's cholesterol level (not that cholesterol causes cancer, either). Eggs are almost all protein and we know of no connection between eating normal dietary levels of protein. So the real conclusion that should sum up this study should have been this:
In the unlikely case that these questionnaires accurately represent what the men who died of prostate cancer ate, and that the memory of consuming eggs actually correlates with an increase in fatal cancers, this association could be explained by the fact that subjects who consumed eggs ate them in meals containing large amounts of dietary carbohydrate and damaged fats, a circumstance our nutritional questionnaire is incapable of detecting. Remember, too, that association is not causation, and ignore this study until someone comes up with one that uses a better study design.
September 21, 2011
The Blood Sugar 101 FaceBook Page is Where You'll Find Tidbits Too Minor for A Blog Post
Yes, I know FB is the greatest time suck ever invented, and that their entire reason for existing is to steal your personal information. But enough of you asked me to set up a page that I did, and it's getting a respectable number of fans.
I'm posting snippets and links there that don't deserve a whole blog post but which are worthy of your attention.
You can post questions there, too, for other fans of the page to comment on.
The FB page is at http://www.facebook.com/pages/Blood-Sugar-101/194439440617073?sk=wall
I'm posting snippets and links there that don't deserve a whole blog post but which are worthy of your attention.
You can post questions there, too, for other fans of the page to comment on.
The FB page is at http://www.facebook.com/pages/Blood-Sugar-101/194439440617073?sk=wall
September 20, 2011
The world is full of people who want to have diabetes
No. I'm not about to rant on about people eating terrible foods that ruin their blood sugar. My topic is something else entirely.
For the past few weeks, for some reason, my email box has been full of letters from people who are desperately hoping that they have diabetes. They don't. In fact, most of them have blood sugar numbers you and I would kill for. When I explain this, they come back saying, "But my mother had diabetes" or "But when I ate an entire chocolate cake my blood sugar rose a whole 30 points. And my fasting blood sugar the next day was 98. That can't be normal!"
Before you dismiss these people as garden variety hypochondriacs, let me explain what's going on.
All these people do have something wrong with them--usually something quite painful or very disturbing. They've been to doctor after doctor who have given them the usual ten minutes of bored attention and then sent them off with a shake of the head or an order for lab tests that come back, almost invariably, with normal values, usually because they are ordering only the standardized tests that turn up the most common medical problems.
So these people email me because they are desperate. They're in pain. Their symtoms are making it hard to go about their daily lives. They've been trolling the internet, scanning for anything that mentions these symptoms, looking for relief, and invariably they end up reading about diabetes because diabetes causes such a wide variety of symptoms. Tiredness, painful feet, stomach pain, ulcers, blurred vision, kidney pain. You name it, someone with diabetes will develop it and post about it somewhere.
So that is why when these people who need help read that doctors do a very poor job of diagnosing diabetes a light goes off in their minds and suddenly they're filled with hope. Maybe that is what is wrong with them, diabetes, and if it is, then there's hope, because once they have a diagnosis they can treat it.
So they email me and I send them off to test their blood sugar, and almost always, when they respond, I have to deliver the news that their blood sugars are completely normal. Whatever is wrong with them, it isn't an obscure, difficult-to-diagnose case of diabetes. Their fasting sugars are under 100 mg/dl. Their sugars don't go over 120 mg/dl after meals. Diabetes is not likely to be causing their symptoms.
You'd be amazed how many people find this upsetting news. They write back to me begging me to consider this or that extra fact. Maybe it isn't diabetes but pre-diabetes. Maybe they hadn't eaten enough carbs when they tested their sugars to be sure. They went low on their glucose tolerance test, isn't that a sign of something?
When I tell them, no, it isn't. They can get testy. I get tempted to tell them to go away because there are dozens of people with diabetes who also need help, and they are taking up my time, but I don't. Because I've been in their shoes--trying to get help for some devastating symptom that doctors wouldn't take seriously and checking out anything that sounds like it might help. I know what a poor job most doctors do diagnosing anything that isn't one of the 85 common conditions they studied in med school.
But there isn't much I can do for them, and I also tell them that whatever is wrong with them, they should rejoice that they don't have diabetes. Because as most you reading this know, even after they diagnose it, most doctors do a lousy job of treating diabetes.
But taking in all these people's miserable experience with doctors who won't diagnose painful conditions, and adding in my own experience with the same, I have to wonder: Why is it that the most sophisticated artificial intelligence systems in the world are devoted almost exclusively to delivering spam that is tailored to your tastes, instead of helping you find out what's wrong with you so you can fix it?
Don't all answer at once. I know it isn't quite that simple.
But if you are one of the masses of people with uncommon, painful, worrying conditions, don't give up. Keep reading and researching. Eventually you may come up with something that should point you in a good direction, and even if you can't go back to your doctor--or a new one, preferably young, recently trained, still enthusiastic, and hungry for new patients, and demand the tests you need to sort out what is going on with your body.
For the past few weeks, for some reason, my email box has been full of letters from people who are desperately hoping that they have diabetes. They don't. In fact, most of them have blood sugar numbers you and I would kill for. When I explain this, they come back saying, "But my mother had diabetes" or "But when I ate an entire chocolate cake my blood sugar rose a whole 30 points. And my fasting blood sugar the next day was 98. That can't be normal!"
Before you dismiss these people as garden variety hypochondriacs, let me explain what's going on.
All these people do have something wrong with them--usually something quite painful or very disturbing. They've been to doctor after doctor who have given them the usual ten minutes of bored attention and then sent them off with a shake of the head or an order for lab tests that come back, almost invariably, with normal values, usually because they are ordering only the standardized tests that turn up the most common medical problems.
So these people email me because they are desperate. They're in pain. Their symtoms are making it hard to go about their daily lives. They've been trolling the internet, scanning for anything that mentions these symptoms, looking for relief, and invariably they end up reading about diabetes because diabetes causes such a wide variety of symptoms. Tiredness, painful feet, stomach pain, ulcers, blurred vision, kidney pain. You name it, someone with diabetes will develop it and post about it somewhere.
So that is why when these people who need help read that doctors do a very poor job of diagnosing diabetes a light goes off in their minds and suddenly they're filled with hope. Maybe that is what is wrong with them, diabetes, and if it is, then there's hope, because once they have a diagnosis they can treat it.
So they email me and I send them off to test their blood sugar, and almost always, when they respond, I have to deliver the news that their blood sugars are completely normal. Whatever is wrong with them, it isn't an obscure, difficult-to-diagnose case of diabetes. Their fasting sugars are under 100 mg/dl. Their sugars don't go over 120 mg/dl after meals. Diabetes is not likely to be causing their symptoms.
You'd be amazed how many people find this upsetting news. They write back to me begging me to consider this or that extra fact. Maybe it isn't diabetes but pre-diabetes. Maybe they hadn't eaten enough carbs when they tested their sugars to be sure. They went low on their glucose tolerance test, isn't that a sign of something?
When I tell them, no, it isn't. They can get testy. I get tempted to tell them to go away because there are dozens of people with diabetes who also need help, and they are taking up my time, but I don't. Because I've been in their shoes--trying to get help for some devastating symptom that doctors wouldn't take seriously and checking out anything that sounds like it might help. I know what a poor job most doctors do diagnosing anything that isn't one of the 85 common conditions they studied in med school.
But there isn't much I can do for them, and I also tell them that whatever is wrong with them, they should rejoice that they don't have diabetes. Because as most you reading this know, even after they diagnose it, most doctors do a lousy job of treating diabetes.
But taking in all these people's miserable experience with doctors who won't diagnose painful conditions, and adding in my own experience with the same, I have to wonder: Why is it that the most sophisticated artificial intelligence systems in the world are devoted almost exclusively to delivering spam that is tailored to your tastes, instead of helping you find out what's wrong with you so you can fix it?
Don't all answer at once. I know it isn't quite that simple.
But if you are one of the masses of people with uncommon, painful, worrying conditions, don't give up. Keep reading and researching. Eventually you may come up with something that should point you in a good direction, and even if you can't go back to your doctor--or a new one, preferably young, recently trained, still enthusiastic, and hungry for new patients, and demand the tests you need to sort out what is going on with your body.
September 1, 2011
My Second Novel Has Just Been Published
No one likes to be defined by their diabetes, not even me. Though I put a lot of time into dealing with it and sharing what I learn with you and other visitors to this site, I have a whole life outside of diabetes which for the past two and a half years has revolved around writing romance novels, since I was fortunate enough to be offered a contract by one of the "Big Six" publishers.
So I'd like to let those of you who enjoy Historical Romances know that my second novel, Star Crossed Seduction is now available.
Based on feedback from people who read the book before publication, Star Crossed Seduction, despite the romance-y title and cover (over which I have no control) also appeals to people who don't usually read romance but enjoy upscale historical fiction, due to the high quality of the writing and the depth of the character development you'll find in its pages. You can learn what it's about, read what reviewers have had to say about it, and find links to where you can buy it online HERE.
Star Crossed Seduction is being stocked in many book stores and some of the larger Walmarts. It is also available in all common e-book formats.
As noted before, my publisher will be contributing a portion of every book sold to the Ovarian Cancer National Alliance, as part of its "K.I.S.S and Teal" campaign which is harnessing the power of Romance novels to reach women readers to raise awareness of this deadly and increasingly common disease.
To celebrate the release of Star Crossed Seduction, I've put together a contest which gives you a chance to win a prize and me a chance to see my book displayed around the country (and the world), which I enjoy because I live in a rural area with almost no bookstores, so I rarely get to see my books on a store shelf live and in person.
All you need to do to enter it is snap a photo of Star Crossed Seduction and either upload it using the form you'll find HERE, email it to me, or post it on the Jenny Brown's Romance Novels page on FaceBook. The winner, chosen at random will get a $25 gift certificate to their favorite online bookstore.
That's all I'll say about the book here, but if you want to keep tabs on my writing career, just "like" the FaceBook page
So I'd like to let those of you who enjoy Historical Romances know that my second novel, Star Crossed Seduction is now available.
Based on feedback from people who read the book before publication, Star Crossed Seduction, despite the romance-y title and cover (over which I have no control) also appeals to people who don't usually read romance but enjoy upscale historical fiction, due to the high quality of the writing and the depth of the character development you'll find in its pages. You can learn what it's about, read what reviewers have had to say about it, and find links to where you can buy it online HERE.
Star Crossed Seduction is being stocked in many book stores and some of the larger Walmarts. It is also available in all common e-book formats.
As noted before, my publisher will be contributing a portion of every book sold to the Ovarian Cancer National Alliance, as part of its "K.I.S.S and Teal" campaign which is harnessing the power of Romance novels to reach women readers to raise awareness of this deadly and increasingly common disease.
To celebrate the release of Star Crossed Seduction, I've put together a contest which gives you a chance to win a prize and me a chance to see my book displayed around the country (and the world), which I enjoy because I live in a rural area with almost no bookstores, so I rarely get to see my books on a store shelf live and in person.
All you need to do to enter it is snap a photo of Star Crossed Seduction and either upload it using the form you'll find HERE, email it to me, or post it on the Jenny Brown's Romance Novels page on FaceBook. The winner, chosen at random will get a $25 gift certificate to their favorite online bookstore.
That's all I'll say about the book here, but if you want to keep tabs on my writing career, just "like" the FaceBook page
August 31, 2011
Six New Diabetes Gene Varients Identified in South Asian Populations
A new study, published in Nature Genetics, emphasizes the diversity of the many physiological breakdowns doctors lump together under the title "Type 2 Diabetes."
You can read a good summary of the study here:
Six New Genetic Variants Linked to Type 2 Diabetes Discovered in South Asians
View the abstract of the actual study here:
Genome-wide association study in individuals of South Asian ancestry identifies six new type 2 diabetes susceptibility loci. Jaspal S. Kooner, et al. Nature Genetics, 2011; DOI: 10.1038/ng.921
The genes involved are GRB14, ST6GAL1, VPS26A, HMG20A, AP3S2 and HNF4A. Of these I recognize HNF4A, which is a gene that has also been identified as the cause of MODY-1 and of the diabetes found in Danish and Ashkenazi Jewish populations. It causes diabetes because when it is damaged, it disturbs the sequence by which a normal pancreatic beta cell is induced to secrete insulin when blood sugars rise over a threshold.
People who have a damaged HNF4A gene respond very strongly to drugs that stimulate insulin secretion because they bypass the stage of the insulin secretion function where HNF4A plays a part. Of these drugs, Prandin and Gliclazide have been found to be the safest. The other sulfonylurea drugs are cheaper, but they are associated with an increased risk of heart attack because they also stimulate a receptor in heart muscle. (Details Here.)
Note: Gliclazide is not sold in the United States. It is marketed as Glizid, Glyloc and Reclide in India and as Diamicron in most other parts of the world.
GRB14 affects insulin receptor signaling and when it is broken it appears to increase insulin resistance.
HMG20A has previously been associated with a greater incidence of diabetes in obese subjects. (Details here.)
This study also identifies a gene that is new to me, ST6GAL1, as affecting the ability to secrete insulin.
ST6GAL1, AP3S2 and VPS26A have something to to with Golgi bodies and do not seem to have been hitherto associated with diabetes. Gogli bodies are parts of the cell that process and assemble proteins for secretion. Perhaps when this gene is damaged insulin secretion is, too. The Nature study abstract reports that ST6GAL1 is associated with impaired insulin secretion but doesn't comment on the others.
What really sticks out here, though, which has been the case with all the genes identified in studies of all populations with "Type 2 diabetes" is that most of the genes identified impact on insulin secretion, NOT insulin resistance and most have nothing to do with obesity.
People mostly seem to get Type 2 diabetes because they don't have a normal ability to secrete insulin. As documented HERE, people with these defective genes often do get fat, but they get fat after their blood sugar starts to rise, probably in response to the ravenous hunger that comes with high blood sugars as they drop back to normal.
As is the case world wide, most people who are obese, even morbidly so don't develop Type 2 diabetes. Only about 10% of any population does, while in some parts of the world, including sections of the U.S. well over 50% of the population is obese.
That said, the question no one in the scientific establishment is asking is this: is it possible that the genetic damage we are seeing which underlies Type 2 diabetes is coming from toxic exposures in our environment? South Asia industrialized very quickly and is notorious for the horrendous environmental conditions that have accompanied this industrialization. We know that herbicides like atrazine, and chemicals used in industrial processes like arsenic, are associated with high rates of both obesity and diabetes. But is anyone looking at what genetic changes these compounds and hundreds of others make?
It's time that we stopped blaming people for causing their diabetes by overeating. Yes, people are overeating, but this is almost always because something major is broken in the built-in systems that regulate appetite. The rise in obesity and in diabetes incidence (which, by the way is a much smaller rise than the rise in obesity), goes back to 1970, which is, coincidentally about a decade after the world replaced wood, metal and glass with plastic for most objects in our immediate environment.
This is not a coincidence, folks. I'm old enough to remember the pre-plastic days, and to remember that people did not walk everywhere or eat small portions back then. That is a fantasy created by the industrial powers who want you to blame yourself for your diabetes and ignore the massive pollution of our environment with the toxic chemicals that make their companies rich.
You can learn about the many chemicals, pharamceuticals, and pollutants that have been linked to causing diabetes HERE.
You can read a good summary of the study here:
Six New Genetic Variants Linked to Type 2 Diabetes Discovered in South Asians
View the abstract of the actual study here:
Genome-wide association study in individuals of South Asian ancestry identifies six new type 2 diabetes susceptibility loci. Jaspal S. Kooner, et al. Nature Genetics, 2011; DOI: 10.1038/ng.921
The genes involved are GRB14, ST6GAL1, VPS26A, HMG20A, AP3S2 and HNF4A. Of these I recognize HNF4A, which is a gene that has also been identified as the cause of MODY-1 and of the diabetes found in Danish and Ashkenazi Jewish populations. It causes diabetes because when it is damaged, it disturbs the sequence by which a normal pancreatic beta cell is induced to secrete insulin when blood sugars rise over a threshold.
People who have a damaged HNF4A gene respond very strongly to drugs that stimulate insulin secretion because they bypass the stage of the insulin secretion function where HNF4A plays a part. Of these drugs, Prandin and Gliclazide have been found to be the safest. The other sulfonylurea drugs are cheaper, but they are associated with an increased risk of heart attack because they also stimulate a receptor in heart muscle. (Details Here.)
Note: Gliclazide is not sold in the United States. It is marketed as Glizid, Glyloc and Reclide in India and as Diamicron in most other parts of the world.
GRB14 affects insulin receptor signaling and when it is broken it appears to increase insulin resistance.
HMG20A has previously been associated with a greater incidence of diabetes in obese subjects. (Details here.)
This study also identifies a gene that is new to me, ST6GAL1, as affecting the ability to secrete insulin.
ST6GAL1, AP3S2 and VPS26A have something to to with Golgi bodies and do not seem to have been hitherto associated with diabetes. Gogli bodies are parts of the cell that process and assemble proteins for secretion. Perhaps when this gene is damaged insulin secretion is, too. The Nature study abstract reports that ST6GAL1 is associated with impaired insulin secretion but doesn't comment on the others.
What really sticks out here, though, which has been the case with all the genes identified in studies of all populations with "Type 2 diabetes" is that most of the genes identified impact on insulin secretion, NOT insulin resistance and most have nothing to do with obesity.
People mostly seem to get Type 2 diabetes because they don't have a normal ability to secrete insulin. As documented HERE, people with these defective genes often do get fat, but they get fat after their blood sugar starts to rise, probably in response to the ravenous hunger that comes with high blood sugars as they drop back to normal.
As is the case world wide, most people who are obese, even morbidly so don't develop Type 2 diabetes. Only about 10% of any population does, while in some parts of the world, including sections of the U.S. well over 50% of the population is obese.
That said, the question no one in the scientific establishment is asking is this: is it possible that the genetic damage we are seeing which underlies Type 2 diabetes is coming from toxic exposures in our environment? South Asia industrialized very quickly and is notorious for the horrendous environmental conditions that have accompanied this industrialization. We know that herbicides like atrazine, and chemicals used in industrial processes like arsenic, are associated with high rates of both obesity and diabetes. But is anyone looking at what genetic changes these compounds and hundreds of others make?
It's time that we stopped blaming people for causing their diabetes by overeating. Yes, people are overeating, but this is almost always because something major is broken in the built-in systems that regulate appetite. The rise in obesity and in diabetes incidence (which, by the way is a much smaller rise than the rise in obesity), goes back to 1970, which is, coincidentally about a decade after the world replaced wood, metal and glass with plastic for most objects in our immediate environment.
This is not a coincidence, folks. I'm old enough to remember the pre-plastic days, and to remember that people did not walk everywhere or eat small portions back then. That is a fantasy created by the industrial powers who want you to blame yourself for your diabetes and ignore the massive pollution of our environment with the toxic chemicals that make their companies rich.
You can learn about the many chemicals, pharamceuticals, and pollutants that have been linked to causing diabetes HERE.
August 26, 2011
Hurricane Preparedness with Diabetes
I'm still hoping the weatherfolk are crying wolf on this one, because the current predictions are that my little town is in the center of the hurricane track and that we can expect week-long power outages. If you don't hear from me after Sunday, you'll know why.
But there's still time to take steps to prepare yourself for the worst, diabetes-style. Here are the basics.
1. Make sure you have enough meds to get yourself through two weeks, because if the pharmacies and gas stations don't have power, you won't be able to fill prescriptions. Ask your pharmacist now for extras if you are in one of the warning areas.
2. If you use insulin, make sure you have some kind of cooler and ice packs so that you can keep your insulin from getting too hot. Don't put insulin directly in contact with freezer packs or ice as cold temperatures will ruin it.
3. Stock up on protein foods that survive without refrigeration like nuts and protein powder so that if you can't cook, you will have something to eat. Avoid salty snack type proteins as your access to water might be limited.
4. Keep your meds and meter right by you with the things you will grab if you have to make a fast exit. I mean VERY fast. Like if the roof is coming down.
Hopefully none of you will need this advice, but you never know when you will be the unlucky person that ends up in the shelter, or in the midst of the flood. Overpreparation is better than the opposite.
Hope you all keep well and safe. . .
But there's still time to take steps to prepare yourself for the worst, diabetes-style. Here are the basics.
1. Make sure you have enough meds to get yourself through two weeks, because if the pharmacies and gas stations don't have power, you won't be able to fill prescriptions. Ask your pharmacist now for extras if you are in one of the warning areas.
2. If you use insulin, make sure you have some kind of cooler and ice packs so that you can keep your insulin from getting too hot. Don't put insulin directly in contact with freezer packs or ice as cold temperatures will ruin it.
3. Stock up on protein foods that survive without refrigeration like nuts and protein powder so that if you can't cook, you will have something to eat. Avoid salty snack type proteins as your access to water might be limited.
4. Keep your meds and meter right by you with the things you will grab if you have to make a fast exit. I mean VERY fast. Like if the roof is coming down.
Hopefully none of you will need this advice, but you never know when you will be the unlucky person that ends up in the shelter, or in the midst of the flood. Overpreparation is better than the opposite.
Hope you all keep well and safe. . .
August 25, 2011
Let's Put our Heads Together: Suggest Diabetes-Friendly Foods for Indian and South Asian Vegetarians
Cutting carbs is quite easy for people eating meat-based western diets, and very effective for cutting carbs. But periodically I hear from people with diabetes diagnoses who for religious or cultural reasons can't eat the kinds of food we westerners do.
My usual suggestions are to eat more cheese, eggs (if allowed), nuts, yogurt, certain dals, papadums, green vegetables, lower carb fruits, and to chose beans over wheat and rice flour-based products. I warn people to avoid soy protein because of it's negative effect on the thyroid. Soy also, because it damages the inner lining of the intestine, makes it much more likely that large proteins from vegetable sources will get into the bloodstream and provoke allergies. (I'm convinced the current increase in gluten allergies we hear so much about of late is a byproduct of the soy that has been in our diet for a generation.)
I'm not sure what the availability is of protein powder in other countries, or if it is affordable. One of the big challenges of a lower carb diet is that all the cheaper foods most people in the world can afford are very high in starch.
So I'm asking for some other suggestions especially from anyone who has made a vegetarian diabetes diet work for more than a year. What are your ideas. Please post them in the comments section.
My usual suggestions are to eat more cheese, eggs (if allowed), nuts, yogurt, certain dals, papadums, green vegetables, lower carb fruits, and to chose beans over wheat and rice flour-based products. I warn people to avoid soy protein because of it's negative effect on the thyroid. Soy also, because it damages the inner lining of the intestine, makes it much more likely that large proteins from vegetable sources will get into the bloodstream and provoke allergies. (I'm convinced the current increase in gluten allergies we hear so much about of late is a byproduct of the soy that has been in our diet for a generation.)
I'm not sure what the availability is of protein powder in other countries, or if it is affordable. One of the big challenges of a lower carb diet is that all the cheaper foods most people in the world can afford are very high in starch.
So I'm asking for some other suggestions especially from anyone who has made a vegetarian diabetes diet work for more than a year. What are your ideas. Please post them in the comments section.
August 15, 2011
Does the High Fat Diet Cause Diabetes? No, But The Onslaught of Bad Research Is Making Me Burn Out.
I've received a torrent of mail about the study recently published in NATURE which claims that eating a "high fat diet" damages beta cells and causes diabetes.
You can read a summary here:
Science Daily: How a High Fat Diet Causes Diabetes
I don't have access to the full article, but I have read (and commented on) dozens of other articles that purport to show that "high fat diets" cause diabetes. And, I have also written at length about the problem of confusing rodent diabetes with human diabetes. Folks, wake up. This was a rodent study!
In every case, the "high fat diet" used in rodent studies is the rodent equivalent of eating a burger with fries and a milkshake. I.e. it's a diet very high in fats, but also very high in carbohydrates--and often that carbohydrate comes in the form of high fructose corn syrup.
In addition, as I've mentioned dozens of times before, rodent metabolisms are very different from human metabolisms because rodents are adapted to eat a very different kind of diet. Rodent diabetes is not human diabetes. "Cures" for diabetic rodents almost never work in humans. Drugs that are safe in rodents harm people.
There is very little research looking into human/rodent differences because rodent research has become a huge specialty in medical research and eliminating reliance on rodent studies would put a lot of very highly paid medical research lab heads out of work. Since it is precisely these highly paid heads of rodent labs who make up the committees who decide who gets research funding, the system is self-perpetuating. Rodent research, no matter how flawed and irrelevant breeds more rodent research.
But that rodent research is not only flawed, it's dangerous. A very rare--and very relevant--study about rodent-human differences was published recently (with almost no mention in the press) and it underlines what I'm talking about.
It found that, in the words of the chief researcher, "...the difference in gene expression between the mouse and the human is very very large." And concluded that the potassium channels acted upon by sulfonylurea drugs are found in completely different places in rodent hearts than they are in human hearts, which means that a drug that is safe for rodents would cause "fatal arrhythmias" in humans. (Which they do. Glipizide, glibenclamide, etc. raise the risk of dying of heart disease over time.)
Science Daily: Human Hearts Respond Differently Than Mouse Hearts to Two Cardiovascular Drugs.
But I can post as much here as I want about flawed studies. It doesn't help. Because the people who read these posts on my blog about misleading research are the people who are already aware of why the research is flawed. It's a classic case of "preaching to the converted."
Analysis of my blog's stats makes it clear that the people who read these kinds of articles are a very small minority of those who read this blog. Almost all the traffic to this blog goes to articles that discuss commonly prescribed drugs and tests. They answer common questions people have who are newly diagnosed. Few who visit this site to find answers to that kind of question read anything but a single post. In short, by now it's clear that the many hours I spend tracking down the details that might offer counterarguments to misleading medical headline news is wasted.
So what it comes down to is this. I can't single-handedly, in my spare time, and for free, counteract the toxic effects an entire medical research establishment funded by multi-billionaire predatory drug companies and backed by armies of doctors who get paid hundreds of thousands of dollars a year to, supposedly, take care of people with diabetes.
Over the last six years I've posted dozens of posts just like this one, many much more detailed, but all pointing out basic flaws and citing other studies that make it very clear that eating carbohydrates is what raises blood sugars, not fats. And that high blood sugars are what cause diabetic complications in humans, not eating fats. I've put an average of 3 hours into each post. Sometimes more. I've answered hundreds of comments and emails from people who read the blog posts and want to know more.
Meanwhile, the misinformation that shapes diabetes treatment gets louder and louder. So it's time for some of the rest of you to get active. If you want things to change, you are going to have to write letters to newspapers and journals, confront doctors, call your TV station, and band together with other people with diabetes to change the way that people with diabetes are treated. If you don't do this, nothing will change, no matter how elegantly I dissect research publications.
There's enough material on this blog by now that a person who wanted to understand any of these new studies could easily apply what has already been explained and do their own analysis. There's plenty you could print out and show your doctor if you took the time.
As far as what I'm going to do it's this. I am done wasting my very limited time reading and commenting on flawed studies. From now on, the only studies I'm going to put time into describing are those that come up with new information that can actually help people with diabetes improve their health.
Such studies are very rare. Please do not email me links to the studies that appear each week "proving" stupid stuff that any reader of this blog and the main Blood Sugar 101 Website knows is bullshit.
Gloria Steinem said something brilliant, reported last week, which sums up exactly how I feel right now.
She said, "The danger of the Internet is cocooning with the like-minded on line -- of sending an email or twitter and confusing that with action -- while the real corporate and military and government centers of power go right on."
People with diabetes need to stop reading things that they agree with and start confronting those centers of power if they want anything to change. Reading elegant articles here might make you feel good, but to change anything you will have to take action. I've already given you hundreds of thousands of words worth of ammunition. Now use it.
You can read a summary here:
Science Daily: How a High Fat Diet Causes Diabetes
I don't have access to the full article, but I have read (and commented on) dozens of other articles that purport to show that "high fat diets" cause diabetes. And, I have also written at length about the problem of confusing rodent diabetes with human diabetes. Folks, wake up. This was a rodent study!
In every case, the "high fat diet" used in rodent studies is the rodent equivalent of eating a burger with fries and a milkshake. I.e. it's a diet very high in fats, but also very high in carbohydrates--and often that carbohydrate comes in the form of high fructose corn syrup.
In addition, as I've mentioned dozens of times before, rodent metabolisms are very different from human metabolisms because rodents are adapted to eat a very different kind of diet. Rodent diabetes is not human diabetes. "Cures" for diabetic rodents almost never work in humans. Drugs that are safe in rodents harm people.
There is very little research looking into human/rodent differences because rodent research has become a huge specialty in medical research and eliminating reliance on rodent studies would put a lot of very highly paid medical research lab heads out of work. Since it is precisely these highly paid heads of rodent labs who make up the committees who decide who gets research funding, the system is self-perpetuating. Rodent research, no matter how flawed and irrelevant breeds more rodent research.
But that rodent research is not only flawed, it's dangerous. A very rare--and very relevant--study about rodent-human differences was published recently (with almost no mention in the press) and it underlines what I'm talking about.
It found that, in the words of the chief researcher, "...the difference in gene expression between the mouse and the human is very very large." And concluded that the potassium channels acted upon by sulfonylurea drugs are found in completely different places in rodent hearts than they are in human hearts, which means that a drug that is safe for rodents would cause "fatal arrhythmias" in humans. (Which they do. Glipizide, glibenclamide, etc. raise the risk of dying of heart disease over time.)
Science Daily: Human Hearts Respond Differently Than Mouse Hearts to Two Cardiovascular Drugs.
But I can post as much here as I want about flawed studies. It doesn't help. Because the people who read these posts on my blog about misleading research are the people who are already aware of why the research is flawed. It's a classic case of "preaching to the converted."
Analysis of my blog's stats makes it clear that the people who read these kinds of articles are a very small minority of those who read this blog. Almost all the traffic to this blog goes to articles that discuss commonly prescribed drugs and tests. They answer common questions people have who are newly diagnosed. Few who visit this site to find answers to that kind of question read anything but a single post. In short, by now it's clear that the many hours I spend tracking down the details that might offer counterarguments to misleading medical headline news is wasted.
So what it comes down to is this. I can't single-handedly, in my spare time, and for free, counteract the toxic effects an entire medical research establishment funded by multi-billionaire predatory drug companies and backed by armies of doctors who get paid hundreds of thousands of dollars a year to, supposedly, take care of people with diabetes.
Over the last six years I've posted dozens of posts just like this one, many much more detailed, but all pointing out basic flaws and citing other studies that make it very clear that eating carbohydrates is what raises blood sugars, not fats. And that high blood sugars are what cause diabetic complications in humans, not eating fats. I've put an average of 3 hours into each post. Sometimes more. I've answered hundreds of comments and emails from people who read the blog posts and want to know more.
Meanwhile, the misinformation that shapes diabetes treatment gets louder and louder. So it's time for some of the rest of you to get active. If you want things to change, you are going to have to write letters to newspapers and journals, confront doctors, call your TV station, and band together with other people with diabetes to change the way that people with diabetes are treated. If you don't do this, nothing will change, no matter how elegantly I dissect research publications.
There's enough material on this blog by now that a person who wanted to understand any of these new studies could easily apply what has already been explained and do their own analysis. There's plenty you could print out and show your doctor if you took the time.
As far as what I'm going to do it's this. I am done wasting my very limited time reading and commenting on flawed studies. From now on, the only studies I'm going to put time into describing are those that come up with new information that can actually help people with diabetes improve their health.
Such studies are very rare. Please do not email me links to the studies that appear each week "proving" stupid stuff that any reader of this blog and the main Blood Sugar 101 Website knows is bullshit.
Gloria Steinem said something brilliant, reported last week, which sums up exactly how I feel right now.
She said, "The danger of the Internet is cocooning with the like-minded on line -- of sending an email or twitter and confusing that with action -- while the real corporate and military and government centers of power go right on."
People with diabetes need to stop reading things that they agree with and start confronting those centers of power if they want anything to change. Reading elegant articles here might make you feel good, but to change anything you will have to take action. I've already given you hundreds of thousands of words worth of ammunition. Now use it.
August 3, 2011
Even with my novels I can't seem to avoid health advocacy.
I've been a bit quiet over the past week as the publication date for my second Avon historical romance is coming up, which mean that I have to put a lot of effort into writing blog posts for various romance blogs in the hope that doing so will motivate readers to buy my book.
You can read a good interview with me wearing my novelist hat--and comment to win a free copy of my first novel, Lord Lightning--HERE.But even when I do something as inconsequential as writing a passionate tale of love and redemption, fate seems to have decreed that it's my job to help people with challenging health issues. Because no sooner was my latest book, Star Crossed Seduction, accepted by my publisher, than I learned that it would be included in a campaign meant to raise awareness of ovarian cancer.
The campaign is called "Kiss and Teal"--referring to the teal blue ribbons used by the Ovarian Cancer National Alliance for its fund raising efforts. The reason for Avon's participation is personal--one of Avon's top editors and one of its biggest bestselling authors both lost their mothers to ovarian cancer recently and together they came up with the idea of using the fact that millions of women buy romance novels to make women more aware of the warning signs of ovarian cancer and of the organization that can help them find the best treatment and clinical trials.
Avon will be donating a portion of the proceeds from every book sold that has the "Kiss and Teal" medallion on the cover, including Star Crossed Seduction, to the Ovarian Cancer National Alliance. Our publicist is also arranging media appearances for us authors--most of whom are far more successful and famous than I am--and gave us an orientation with someone from the Alliance who taught us a lot about this deadly disease. This will make it possible for us to tell a larger audience about the warning signs of this cancer that is the fifth most common cancer killer of women.
My college roommate died of a form of cancer closely related to ovarian cancer at the much-too-young age of 28. Her death was one of the first events that made me aware of the dangers of pharmaceutical drugs, because she was a DES daughter. Her mother had been prescribed a hormone pill that was supposed to avoid pregnancy complications. Instead, it caused terrible damage to the children of those who took it, including fatal cancers like those that killed my roommate and reproductive tract anomalies. It is still causing significant problems in surviving DES daughters--they have a greater risk of ovarian cancer--and in the grandchildren of the women who took it.
Every woman should read about the warning symptoms of ovarian cancer which you'll find HERE. If you are a DES daughter, it is even more important that you do this.
This early experience with a drug whose negative impacts took decades to emerge should have made doctors think about the long term impact of drugs they prescribe. DES was prescribed in the late 1940s. But obviously, it hasn't. Hormones were new and exciting in the 1940s in the same way that drugs that block receptors and turn off gene expression are in this decade.
Which is why, as long term readers of this blog know, I continue to worry about the long term impact of prescribing DPP-4 inhibitors like Januvia and Onglyza that turn off a gene the body uses to fight ovarian cancer, melanoma, prostate cancer and lung cancer. (Details HERE and HERE).
Just this week, a friend of the blog sent me a study, published back in February in the journal, Gasteroenterology, and completely ignored by the health media, which found a much higher incidence of pancreatic and thyroid cancers among people taking Januvia and Byetta. You can read it HERE.
Though there are issues with the methodology used--which the authors are very frank in describing--there is no question that, as we learned from the artificial hormone DES years ago, drugs that use novel mechanisms that mess with hormones (like GLP-1) and supress gene expression(as does Januvia, Onglyza, etc.) may very well cause cancer--and they will do it after a much longer time period has passed than the brief two or three years over which which drug acceptance studies last. (After a drug is approved there is no significant tracking of its subsequent connection with cancers, and the database that attempts to collect this data is, as the Gastroenterology study discusses, quite limited and flawed.)
The lesson is clear. Drugs have short term benefits that may be much easier to see than the long term disturbances they make in our body that might kill us. Messing with systems we don't really understand--like the human body--is going to produce unexpected results.
So here's a bit of ovarian cancer awareness for those of you with diabetes--and you don't have to buy my novel to benefit from it, though of course I hope you will. Anyone with a family history of ovarian cancer should stay away from any drug that inhibits DPP-4. It will take 20 years for it to become clear what the impact of turning off this tumor suppressing gene really is.
But it is often hard to know if you have a family history of ovarian cancer, due to the huge burden of shame and silence that kept women of earlier generations from telling anyone that they suffered from this kind of cancer. So if you have had female relatives who died of any mysterious cancers, you should be particularly careful about what drugs you take, and it is essential that you NOT take any of the DPP-4 inhibitors that make it easier for a preexisting ovarian cancer to spread.
Metformin, fortunately, seems to have a protective effect against cancer, which is why I, a melanoma survivor, take it even when my blood sugars are in very good control.
You can read a good interview with me wearing my novelist hat--and comment to win a free copy of my first novel, Lord Lightning--HERE.But even when I do something as inconsequential as writing a passionate tale of love and redemption, fate seems to have decreed that it's my job to help people with challenging health issues. Because no sooner was my latest book, Star Crossed Seduction, accepted by my publisher, than I learned that it would be included in a campaign meant to raise awareness of ovarian cancer.
The campaign is called "Kiss and Teal"--referring to the teal blue ribbons used by the Ovarian Cancer National Alliance for its fund raising efforts. The reason for Avon's participation is personal--one of Avon's top editors and one of its biggest bestselling authors both lost their mothers to ovarian cancer recently and together they came up with the idea of using the fact that millions of women buy romance novels to make women more aware of the warning signs of ovarian cancer and of the organization that can help them find the best treatment and clinical trials.
Avon will be donating a portion of the proceeds from every book sold that has the "Kiss and Teal" medallion on the cover, including Star Crossed Seduction, to the Ovarian Cancer National Alliance. Our publicist is also arranging media appearances for us authors--most of whom are far more successful and famous than I am--and gave us an orientation with someone from the Alliance who taught us a lot about this deadly disease. This will make it possible for us to tell a larger audience about the warning signs of this cancer that is the fifth most common cancer killer of women.
My college roommate died of a form of cancer closely related to ovarian cancer at the much-too-young age of 28. Her death was one of the first events that made me aware of the dangers of pharmaceutical drugs, because she was a DES daughter. Her mother had been prescribed a hormone pill that was supposed to avoid pregnancy complications. Instead, it caused terrible damage to the children of those who took it, including fatal cancers like those that killed my roommate and reproductive tract anomalies. It is still causing significant problems in surviving DES daughters--they have a greater risk of ovarian cancer--and in the grandchildren of the women who took it.
Every woman should read about the warning symptoms of ovarian cancer which you'll find HERE. If you are a DES daughter, it is even more important that you do this.
This early experience with a drug whose negative impacts took decades to emerge should have made doctors think about the long term impact of drugs they prescribe. DES was prescribed in the late 1940s. But obviously, it hasn't. Hormones were new and exciting in the 1940s in the same way that drugs that block receptors and turn off gene expression are in this decade.
Which is why, as long term readers of this blog know, I continue to worry about the long term impact of prescribing DPP-4 inhibitors like Januvia and Onglyza that turn off a gene the body uses to fight ovarian cancer, melanoma, prostate cancer and lung cancer. (Details HERE and HERE).
Just this week, a friend of the blog sent me a study, published back in February in the journal, Gasteroenterology, and completely ignored by the health media, which found a much higher incidence of pancreatic and thyroid cancers among people taking Januvia and Byetta. You can read it HERE.
Though there are issues with the methodology used--which the authors are very frank in describing--there is no question that, as we learned from the artificial hormone DES years ago, drugs that use novel mechanisms that mess with hormones (like GLP-1) and supress gene expression(as does Januvia, Onglyza, etc.) may very well cause cancer--and they will do it after a much longer time period has passed than the brief two or three years over which which drug acceptance studies last. (After a drug is approved there is no significant tracking of its subsequent connection with cancers, and the database that attempts to collect this data is, as the Gastroenterology study discusses, quite limited and flawed.)
The lesson is clear. Drugs have short term benefits that may be much easier to see than the long term disturbances they make in our body that might kill us. Messing with systems we don't really understand--like the human body--is going to produce unexpected results.
So here's a bit of ovarian cancer awareness for those of you with diabetes--and you don't have to buy my novel to benefit from it, though of course I hope you will. Anyone with a family history of ovarian cancer should stay away from any drug that inhibits DPP-4. It will take 20 years for it to become clear what the impact of turning off this tumor suppressing gene really is.
But it is often hard to know if you have a family history of ovarian cancer, due to the huge burden of shame and silence that kept women of earlier generations from telling anyone that they suffered from this kind of cancer. So if you have had female relatives who died of any mysterious cancers, you should be particularly careful about what drugs you take, and it is essential that you NOT take any of the DPP-4 inhibitors that make it easier for a preexisting ovarian cancer to spread.
Metformin, fortunately, seems to have a protective effect against cancer, which is why I, a melanoma survivor, take it even when my blood sugars are in very good control.
July 11, 2011
Healthy Whole Grains, Just as Healthy as Pepsi--One Reader Reports
As readers of this blog know, there's nothing I like better than data, and there's no data I like better than the blood sugar meter test results that tell an individual what foods they can eat without raising their blood sugar over the level that causes complications (which is roughly 140 mg/dl or 7.7 mmol/L).
So I was intrigued when a Richard Smith, a friend of the blog, sent me the following report on his personal study as to how what dietitians like to call "healthy whole grains" affected his blood sugar, using as a control a 12 ounce glass of regular Pepsi.
Richard gave me permission to share his data, so here it is:
=======
This was his brilliant counter-argument to the advice of ADA-associated nutritionist, Hope Warshaw, whose recommendations have been getting more attention on the interwebs than they deserve.
But rather than rage against the so called professionals who give toxic advice, I'd just like to remind everyone reading that your blood sugar meter is the most powerful diabetes-correction tool you own. Test your blood sugar after you eat a food you've been told is healthy to find out if it really is "diabetes friendly" for you.
There is solid research that points out that heart disease gets going when blood sugars rise over 155 mg/dl (8.6 mmol/L) one hour after meals. (Details HERE.)
Obviously the "healthy whole grains" beloved by doctors, nutritionists, and the American Diabetes Association failed to pass the "diabetes friendly" test for this experimenter.
So consider no food healthy unless your own one hour post-meal numbers after eating eating them in a meal comes in under 155 mg/dl (8.6 mmol/L) and, ideally, under the 140 mg/dl (7.7 mmol/L) level that, maintained over time, usually results in an A1c in the 5% range.
So I was intrigued when a Richard Smith, a friend of the blog, sent me the following report on his personal study as to how what dietitians like to call "healthy whole grains" affected his blood sugar, using as a control a 12 ounce glass of regular Pepsi.
Richard gave me permission to share his data, so here it is:
The New Pepsi Challenge results (Pepsi vs. whole grains)
Food |
Net carbs |
BG before eating |
BG at 1 hour |
BG at 90 minutes |
BG at 2 hours |
12oz Pepsi |
42g |
89 |
156 |
127 |
101 |
Oatmeal and milk |
40g |
113 |
163 |
N/A |
92 |
Whole wheat bread |
48g |
93 |
141 |
142 |
107 |
Whole wheat toast |
36g |
103 |
173 |
143 |
94 |
Testing was done with a NovaMax meter over a two day period.
He adds: It is no surprise that meals with whole grain starches have about the same effect on my blood sugar as drinking a 12oz Pepsi.
=======
This was his brilliant counter-argument to the advice of ADA-associated nutritionist, Hope Warshaw, whose recommendations have been getting more attention on the interwebs than they deserve.
But rather than rage against the so called professionals who give toxic advice, I'd just like to remind everyone reading that your blood sugar meter is the most powerful diabetes-correction tool you own. Test your blood sugar after you eat a food you've been told is healthy to find out if it really is "diabetes friendly" for you.
There is solid research that points out that heart disease gets going when blood sugars rise over 155 mg/dl (8.6 mmol/L) one hour after meals. (Details HERE.)
Obviously the "healthy whole grains" beloved by doctors, nutritionists, and the American Diabetes Association failed to pass the "diabetes friendly" test for this experimenter.
So consider no food healthy unless your own one hour post-meal numbers after eating eating them in a meal comes in under 155 mg/dl (8.6 mmol/L) and, ideally, under the 140 mg/dl (7.7 mmol/L) level that, maintained over time, usually results in an A1c in the 5% range.
July 6, 2011
Jimmy Moore Podcast Interview with Jenny Ruhl July 7th,
I just found out that Jimmy Moore is posting the conversation we had last month tomorrow on his Living La Vida Low Carb show. You'll find the podcast here:
http://www.thelivinlowcarbshow.com/shownotes/
If you have any questions after you hear it, feel free to post them here.
http://www.thelivinlowcarbshow.com/shownotes/
If you have any questions after you hear it, feel free to post them here.
June 24, 2011
Idiotically Dangerous Diet "Reverses Diabetes" but So Does Moderate Carb Restriction Without Calorie Restriction
UPDATE: 2017
Though Dr. Taylor said he was going to publish a follow up to the "landmark" study discussed below that got so much press, but as of 2017, none has ever appeared. My guess is that no follow up was published because it was impossible for people with Type 2 diabetes to maintain blood sugar control for more than a year or two using the extreme diet strategy he promoted. It is also likely they ended up much fatter than they started because that is what happens to people who go on starvation diets, which this is, even with medical supervision.
____
Original Post:
All last night and this morning my email inbox has been filling up with notes pointing me to this story:
Crash Course Diet Reverses Type 2 Diabetes in a week.
It is yet another example of the tragically flawed pseudo-science that damages the health of people with diabetes.
There's no mystery here, nor is the effect reported a result of "reducing fat in the pancreas" as the doctor who came up with this "cure" suggests. All he has done is craft a "balanced" diet that has so few calories it is also low in carbohydrates.
As all my readers know, most people with Type 2 diabetes--especially those recently diagnosed--can recover normal blood sugar control simply by cutting back their carbohydrate intake to somewhere between 30 and 100 grams of carbohydrate a day. The actual number varies with the size of the person, their gender (men can usually tolerate more carb), and the ability of the individual's beta cells to secrete insulin.
But a low carb diet with normal calories is a high fat diet, and doctors have been brainwashed to believe that high fat/low carb diets cause heart disease. They don't. You can read the research that has proven this HERE.
But doctors don't have the time to keep up with nutritional research, so they still believe it. And because of their fat phobia, the only way doctors can feel comfortable prescribing a very low carb diet is by pretending they aren't prescribing one--which they do by prescribing "balanced" diets, one like the one reported here, where the calories are so low that a diet that includes 33% of calories in the form of carbohydrate becomes a low carb diet.
Starvation Diets Like This One Are Dangerous
In fact, there's nothing new or healthy about the low cal diet this doctor has come up with. The starvation diet is well understood--and very expensive. It can only be pursued under the supervision of paid medical staff that includes trained nutritionists because cutting calories that low on your own can be extremely dangerous both to your body and your mind.
The classic research on ultra low calorie diets, the starvation research conducted by Dr. Ancel Keys during WWII showed that people eating very low calorie diets developed psychoses (i.e. severe mental illness) at a surprisingly high rate, as well as many other important health problems. Poorly crafted medically supervised low fat starvation diets have caused deaths in the past.
Very low calorie diets of all kinds are extremely hard on the heart because they can't supply enough protein to repair muscle, so the body ends up cannibalizing the heart muscle.
Even with careful nutritional supervision, when calories are that low, the thyroid and other parts of the system that regulate metabolism slow in order to make the best use of every available bit of energy and the result is that after a month or two on the very low calorie diet, the person who dieted so unwisely will find themselves gaining weight on a caloric intake so low that it should be a weight loss diet for someone their size.
Partially this is because some metabolic slowdown occurs in anyone who loses a significant amount of weight on any diet. I discussed this in a blog post that highlighted Dr. Liebel's research about metabolic slow down with weight loss.
But extreme calorie deprivation seems to intensify this effect. Some years ago, many denizens of the Low Carb Friends diet discussion board fell for scam diet, the so-called Kimkins diet, which was a low carb, low fat diet which was effective in taking off weight fast (and cutting blood sugar) because starvation diets WILL do that, but which also left quite a few of them with metabolisms so damaged that they started gaining weight eating as little as 1200 calories a day, their hair fell out, and they developed mood disorders and other severe deficiency problems. It took several years for some of them to get their health back.
The Gastric Bypass Model For the Diet is Misunderstood
The doctor in this study purporting to "reverse diabetes" justifies his approach by explaining that it duplicates what people eat when they have had gastric bypass, but what is forgotten is that people with gastric bypass often develop long lasting and severe nutritional deficiencies. The restricted diet enforced by weight loss surgery also appears to cause an unexpectedly high rate of suicide which goes along with what we know about severe calorie restriction causing severe mood disorders. This, sadly, is a subject you won't learn about in the enthusiastic plugs for it you read in the media which are supplied by press agents working for bariatric surgeons. Details HERE. Note that this important epidemiological study, published last September, got NO play in the health media.
What is also forgotten is that the research suggests that the real reason some people "reverse their diabetes" after gastric bypass is that they can no longer tolerate carbohydrates and will experience projectile vomiting if they eat enough carbohydrate to raise their blood sugar. Weight Loss Surgery therefore forces them to eat a very low carbohydrate diet and THAT is what "reverses" their diabetes.
Starvation Diets Like This One Are Unnecessary: It's All About The Carbs
What most doctors don't know and won't be told by the surgeons who are profiting so mightily from weight loss surgery is that people who "reverse" or "cure" their diabetes with weight loss surgery get their diabetes right back as soon as their stomachs stretch out to where they can eat enough carbohydrates to raise their blood sugar again. (You'll find studies proving this HERE.)
Clearly, there isn't any magic in the surgery or in calorie restriction that is what is supposedly "reversing" diabetes. Blood sugars come down only because these approaches remove the one component of the diet that raises blood sugars into the diabetic range: carbohydrates.
But as thousands of people with diabetes have learned, you can get the same effect by eating a diet that contains normal amounts of calories if you are willing to removed carbohydrates and replace them with healthy fats and protein. And when you do this you don't risk developing nutritional deficiencies or the possibility of developing a severe mood disorder.
It's Time for the Annual ADA Conference. Vendor-Sponsored "Research" Will Be Swamping the Health Media
It's not accidental that this study was published yesterday, tomorrow marks the beginning of the American Diabetes Association's so-called "Scientific Sessions". This is the annual conference where those who make their living selling goods and services to people promote their wares to doctors using poorly designed corporate-funded studies that twist the data to prove whatever will make the sponsor the most money.
High profile doctors the drug companies call "thought leaders"--each of whom receives huge fees from the drug companies--will give talks to their peers that purport to explain the mechanics of diabetes but which really do nothing but convince other doctors that the only treatments they should give people with diabetes are the most expensive new drugs.
So over this next week expect to see a lot of media reports about miraculous new drugs. You'll probably also be hearing a lot of praise for the miraculous effects of weight loss surgery, since the weight loss surgeons seem to have paid "charitable contributions" to the ADA to have bought a seat at the table previously dominated by drug merchants.
You'll see headlines suggesting that high fat diets cause diabetes in humans--all of which will have been conducted in rats bred to develop diabetes on high fat diets. (You can read more about this questionable methodology HERE.)
You'll read about dozens of "cures" of diabetes--all conducted in mice whose diabetes is caused by everything except the genes that cause diabetes in humans.
What you won't find at the ADA Scientific Sessions, ever, is any significant participation by people who HAVE diabetes and who have controlled it using strategies that don't cost an arm and a leg. Like carbohydrate restriction. The ADA has been fighting for decades for the right of its corporate food company sponsors to sell starchy breakfast cereal, soups, bread, and over processed juices to diabetics as "health food" for diabetics, and it will keep on doing it.
But the truth for most of us real people with diabetes who have maintained normal blood sugars for years without resorting to radical surgery or diets is that cutting way back on the carbohydrates we eat at meals will dramatically lower our blood sugars.
You can easily test this proposition at home. If you are new to this blog I urge you to read this page HERE and try the technique it suggests.
NOTE: Please click on the Comments link below to read more information and discussion based on the full text of the published study.
Though Dr. Taylor said he was going to publish a follow up to the "landmark" study discussed below that got so much press, but as of 2017, none has ever appeared. My guess is that no follow up was published because it was impossible for people with Type 2 diabetes to maintain blood sugar control for more than a year or two using the extreme diet strategy he promoted. It is also likely they ended up much fatter than they started because that is what happens to people who go on starvation diets, which this is, even with medical supervision.
____
Original Post:
All last night and this morning my email inbox has been filling up with notes pointing me to this story:
Crash Course Diet Reverses Type 2 Diabetes in a week.
It is yet another example of the tragically flawed pseudo-science that damages the health of people with diabetes.
There's no mystery here, nor is the effect reported a result of "reducing fat in the pancreas" as the doctor who came up with this "cure" suggests. All he has done is craft a "balanced" diet that has so few calories it is also low in carbohydrates.
As all my readers know, most people with Type 2 diabetes--especially those recently diagnosed--can recover normal blood sugar control simply by cutting back their carbohydrate intake to somewhere between 30 and 100 grams of carbohydrate a day. The actual number varies with the size of the person, their gender (men can usually tolerate more carb), and the ability of the individual's beta cells to secrete insulin.
But a low carb diet with normal calories is a high fat diet, and doctors have been brainwashed to believe that high fat/low carb diets cause heart disease. They don't. You can read the research that has proven this HERE.
But doctors don't have the time to keep up with nutritional research, so they still believe it. And because of their fat phobia, the only way doctors can feel comfortable prescribing a very low carb diet is by pretending they aren't prescribing one--which they do by prescribing "balanced" diets, one like the one reported here, where the calories are so low that a diet that includes 33% of calories in the form of carbohydrate becomes a low carb diet.
Starvation Diets Like This One Are Dangerous
In fact, there's nothing new or healthy about the low cal diet this doctor has come up with. The starvation diet is well understood--and very expensive. It can only be pursued under the supervision of paid medical staff that includes trained nutritionists because cutting calories that low on your own can be extremely dangerous both to your body and your mind.
The classic research on ultra low calorie diets, the starvation research conducted by Dr. Ancel Keys during WWII showed that people eating very low calorie diets developed psychoses (i.e. severe mental illness) at a surprisingly high rate, as well as many other important health problems. Poorly crafted medically supervised low fat starvation diets have caused deaths in the past.
Very low calorie diets of all kinds are extremely hard on the heart because they can't supply enough protein to repair muscle, so the body ends up cannibalizing the heart muscle.
Even with careful nutritional supervision, when calories are that low, the thyroid and other parts of the system that regulate metabolism slow in order to make the best use of every available bit of energy and the result is that after a month or two on the very low calorie diet, the person who dieted so unwisely will find themselves gaining weight on a caloric intake so low that it should be a weight loss diet for someone their size.
Partially this is because some metabolic slowdown occurs in anyone who loses a significant amount of weight on any diet. I discussed this in a blog post that highlighted Dr. Liebel's research about metabolic slow down with weight loss.
But extreme calorie deprivation seems to intensify this effect. Some years ago, many denizens of the Low Carb Friends diet discussion board fell for scam diet, the so-called Kimkins diet, which was a low carb, low fat diet which was effective in taking off weight fast (and cutting blood sugar) because starvation diets WILL do that, but which also left quite a few of them with metabolisms so damaged that they started gaining weight eating as little as 1200 calories a day, their hair fell out, and they developed mood disorders and other severe deficiency problems. It took several years for some of them to get their health back.
The Gastric Bypass Model For the Diet is Misunderstood
The doctor in this study purporting to "reverse diabetes" justifies his approach by explaining that it duplicates what people eat when they have had gastric bypass, but what is forgotten is that people with gastric bypass often develop long lasting and severe nutritional deficiencies. The restricted diet enforced by weight loss surgery also appears to cause an unexpectedly high rate of suicide which goes along with what we know about severe calorie restriction causing severe mood disorders. This, sadly, is a subject you won't learn about in the enthusiastic plugs for it you read in the media which are supplied by press agents working for bariatric surgeons. Details HERE. Note that this important epidemiological study, published last September, got NO play in the health media.
What is also forgotten is that the research suggests that the real reason some people "reverse their diabetes" after gastric bypass is that they can no longer tolerate carbohydrates and will experience projectile vomiting if they eat enough carbohydrate to raise their blood sugar. Weight Loss Surgery therefore forces them to eat a very low carbohydrate diet and THAT is what "reverses" their diabetes.
Starvation Diets Like This One Are Unnecessary: It's All About The Carbs
What most doctors don't know and won't be told by the surgeons who are profiting so mightily from weight loss surgery is that people who "reverse" or "cure" their diabetes with weight loss surgery get their diabetes right back as soon as their stomachs stretch out to where they can eat enough carbohydrates to raise their blood sugar again. (You'll find studies proving this HERE.)
Clearly, there isn't any magic in the surgery or in calorie restriction that is what is supposedly "reversing" diabetes. Blood sugars come down only because these approaches remove the one component of the diet that raises blood sugars into the diabetic range: carbohydrates.
But as thousands of people with diabetes have learned, you can get the same effect by eating a diet that contains normal amounts of calories if you are willing to removed carbohydrates and replace them with healthy fats and protein. And when you do this you don't risk developing nutritional deficiencies or the possibility of developing a severe mood disorder.
It's Time for the Annual ADA Conference. Vendor-Sponsored "Research" Will Be Swamping the Health Media
It's not accidental that this study was published yesterday, tomorrow marks the beginning of the American Diabetes Association's so-called "Scientific Sessions". This is the annual conference where those who make their living selling goods and services to people promote their wares to doctors using poorly designed corporate-funded studies that twist the data to prove whatever will make the sponsor the most money.
High profile doctors the drug companies call "thought leaders"--each of whom receives huge fees from the drug companies--will give talks to their peers that purport to explain the mechanics of diabetes but which really do nothing but convince other doctors that the only treatments they should give people with diabetes are the most expensive new drugs.
So over this next week expect to see a lot of media reports about miraculous new drugs. You'll probably also be hearing a lot of praise for the miraculous effects of weight loss surgery, since the weight loss surgeons seem to have paid "charitable contributions" to the ADA to have bought a seat at the table previously dominated by drug merchants.
You'll see headlines suggesting that high fat diets cause diabetes in humans--all of which will have been conducted in rats bred to develop diabetes on high fat diets. (You can read more about this questionable methodology HERE.)
You'll read about dozens of "cures" of diabetes--all conducted in mice whose diabetes is caused by everything except the genes that cause diabetes in humans.
What you won't find at the ADA Scientific Sessions, ever, is any significant participation by people who HAVE diabetes and who have controlled it using strategies that don't cost an arm and a leg. Like carbohydrate restriction. The ADA has been fighting for decades for the right of its corporate food company sponsors to sell starchy breakfast cereal, soups, bread, and over processed juices to diabetics as "health food" for diabetics, and it will keep on doing it.
But the truth for most of us real people with diabetes who have maintained normal blood sugars for years without resorting to radical surgery or diets is that cutting way back on the carbohydrates we eat at meals will dramatically lower our blood sugars.
You can easily test this proposition at home. If you are new to this blog I urge you to read this page HERE and try the technique it suggests.
NOTE: Please click on the Comments link below to read more information and discussion based on the full text of the published study.
June 9, 2011
Avandia is sufficient to explain the excess deaths in ACCORD--the study being used to argue that normal blood sugars are dangerous.
If your doctor is telling you that research has "proved" that lowering blood sugars below an A1c of 6.5% is "dangerous" print out this letter, which was just published in the New England Journal of Medicine, and demand that your doctor read it:
Intensive Glucose Lowering and Cardiovascular Outcomes N Engl J Med 2011; 364:2263-2264 June 9, 2011
If you can't get the full letter to display here are the salient statements it contains. The quote refers to the ACCORD study where the intensive-therapy group was the group of people with Type 2 Diabetes who were urged to get their A1c down below 6.5%:
This is a VERY important point. The ACCORD results have been used to justify doctors' and insurers' refusal to give people with Type 2 the medications and blood sugar meters they need to achieve normal blood sugars. Since it was published and interpreted as meaning that intensive efforts to your lower blood sugar will result in your having a higher risk of experiencing a heart attack I have heard from dozens of people whose doctors cautioned them to keep their A1c at 7.0% or higher and based their conclusions on this study.
This kind of toxic advice has been given to many thousands of people with Type 2 diabetes who will go on to suffer unnecessary diabetic complications that become inevitable at A1cs over 6.0% .
My guess is that the makers of Avandia had something to do with the fact that the health media blamed the excess heart attacks that occurred in the lower A1c group on their lower blood sugar rather than on these subjects' taking a drug that raises the risk of heart attacks.
It is odd, isn't it, that these journals did not make public in accessible form the numbers linking this exposure to Avandia with the excess deaths in ACCORD until now, after Avandia has been, for all practical purposes, taken off the market.
Coinicidental? I think not. Not with the power GlaxoSmithKline wields with its huge advertising budget and its research grants. No media outlet is going to risk losing those full two- and three- page drug company spreads just to save the limbs, vision and kidneys of a bunch of fat old people with diabetes.
Shame on the mainstream medical journals for not making this information public when they first knew of it.
Intensive Glucose Lowering and Cardiovascular Outcomes N Engl J Med 2011; 364:2263-2264 June 9, 2011
If you can't get the full letter to display here are the salient statements it contains. The quote refers to the ACCORD study where the intensive-therapy group was the group of people with Type 2 Diabetes who were urged to get their A1c down below 6.5%:
44.7% of subjects in the intensive-therapy group, as compared with 25.2% of patients in the standard-therapy group, received rosiglitazone [Avandia] just before the study transition date. According to the 2008 article summarizing the results of the ACCORD trial up to the point of protocol transition, 91.2% of subjects in the intensive-therapy group, as compared with 57.5% of patients in the standard-therapy group, had received rosiglitazone.The signers of this letter are Almut G. Winterstein, Ph.D., University of Florida, Gainesville, FL, Susan R. Heckbert, M.D., Ph.D., University of Washington, Seattle, WA, and Morris Schambelan, M.D. University of California, San Francisco, CA.
[snip]
Although other differences in drug exposure warrant further analysis, we think that the authors[of the ACCORD publications] should consider (and address in a secondary analysis) the role of rosiglitazone in the excess deaths from cardiovascular causes, especially in the absence of biologic plausibility of a glucose-mediated effect. Given unbalanced exposure, we think that the ACCORD trial is inconclusive and that the recommendation to abandon lower glucose targets is not supported and has unknown consequences for the long-term management of diabetes. [Emphasis mine]
This is a VERY important point. The ACCORD results have been used to justify doctors' and insurers' refusal to give people with Type 2 the medications and blood sugar meters they need to achieve normal blood sugars. Since it was published and interpreted as meaning that intensive efforts to your lower blood sugar will result in your having a higher risk of experiencing a heart attack I have heard from dozens of people whose doctors cautioned them to keep their A1c at 7.0% or higher and based their conclusions on this study.
This kind of toxic advice has been given to many thousands of people with Type 2 diabetes who will go on to suffer unnecessary diabetic complications that become inevitable at A1cs over 6.0% .
My guess is that the makers of Avandia had something to do with the fact that the health media blamed the excess heart attacks that occurred in the lower A1c group on their lower blood sugar rather than on these subjects' taking a drug that raises the risk of heart attacks.
It is odd, isn't it, that these journals did not make public in accessible form the numbers linking this exposure to Avandia with the excess deaths in ACCORD until now, after Avandia has been, for all practical purposes, taken off the market.
Coinicidental? I think not. Not with the power GlaxoSmithKline wields with its huge advertising budget and its research grants. No media outlet is going to risk losing those full two- and three- page drug company spreads just to save the limbs, vision and kidneys of a bunch of fat old people with diabetes.
Shame on the mainstream medical journals for not making this information public when they first knew of it.
June 7, 2011
News You Missed. WHI: Low Fat Diet Dramatically Worsens Diabetic Blood Sugars
Over the past month the media have been busy doing what they do best--reporting bady designed animal research as if it were human research. As a result we read "A high-fat diet during pregnancy may program a woman's baby for future diabetes, even if she herself is not obese or diabetic." This headline multiplied through the web appearing on dozens of newspaper sites.
Only by reading the full article do we learn that the researchers concluded this after an undisclosed, but probably low, number of "obesity-resistant rats" were "fed... either a high-fat or a control diet from the first day of gestation."
Rodents have evolved to eat a very different diet than humans and don't do well on high fat diets. They have very different pancreases and enzyme function than humans. And, of course, the "high fat diet" used in rat research is also a high carbohydrate diet. But that didn't deter the media from reporting this finding as if it were a human study.
Another study that was reported in the media claimed that "Pregnant women who tuck into fatty foods are at greater risk of having a stillbirth."
Further reading reveals that "The team studied two dozen pregnant Japanese macaque monkeys, an animal that has a placental structure similar to humans." Not mentioned here is the fact that Macaques, like other monkeys, have evolved to eat a very different diet from humans. They live mostly on fruits, herbs, and seeds, seasoned with the occasional insect, and can't tolerate the diet of fatty meat that humans evolved to not only tolerate but flourish on.
These are just a few of the animal research studies demonizing the impact of fat on females that appeared over the past month. But what about research that looked at the impact of fatty diets on female humans?
There was , it turns out, a blockbuster human study published this past month--an important study that described the impact of a low fat diet on real, live human women. Shockingly, it received no mention in the press at all.
But what a study it was! Unlike the studies that featured a dozen monkeys or a lab full of rats, this study tracked the outcomes for 2,263 human women, whose diet, blood sugar, and insulin were tracked for six full years.
And what it found was this: Low fat diets harm women with diabetes. Here's the study:
Effects of a low-fat dietary intervention on glucose, insulin, and insulin resistance in the Women's Health Initiative (WHI) Dietary Modification trial Shikany JM, et al. Am J Clin Nutr. 2011 May 11. [Epub ahead of print]
To understand how important a result this was, we need to back track a little and remind ourselves of what the largest and best designed study of the low fat diet has already proven, which is that in almost 49,000 middle aged women, tracked over eight years, the low fat diet was shown to have zero effect on preventing heart disease or stroke. None. Nada. Zip.
The earlier publication describing the WHI findings concluded
Low-Fat Dietary Pattern and Risk of Cardiovascular Disease:The Women's Health Initiative Randomized Controlled Dietary Modification Trial Barbara V. Howard et al. JAMAVol. 295 No. 6, February 8, 2006
When this result hit the press in 2006, the media and the high profile doctors who have been promoting the low fat diet for decades responded by asserting that the diet used in the study must not have been low enough in fat, or that the study hadn't lasted long enough to demonstrate the benefits that the low fat diet must have. No one was willing to admit that maybe the study had proven what it looked like it proved--that the low fat diet was a useless intervention.
Doctors continue to recommend low fat diets. Dietitians continue to warn people with diabetes about the dangers of eating fat.
But now, this lastest analysis of the WHI data shows just how wrong-headed they are, because what the researches did here is to take the further step of analyzing the results for the subset of women for whom they had blood sugar measurements at the start of the study.
What they found was that for women with diabetes, the low fat diet wasn't just useless, it was dangerous, because it raised their blood sugar significantly--and I don't mean just statistically significantly. I mean it raised it a lot.
In the study's words, "...diabetic women had an increase in glucose that was 7.9 ± 20.3 mg/dL greater in the DM [diabetes]-I[ntervention, i.e. low fat diet group] than in the DM-C[ontrol] group (P for interaction <0.001).
In short, women with diabetes who didn't eat a low fat diet ended up with much better blood sugars, even though both groups were eating a high carbohydrate diet!
Since these were diabetic women who were likely to be taking medications to lower their blood sugar, the rise in blood sugar seen on the low fat diet is worse than it looks, because it takes into account the higher doses of medications they were probably taking.
Science doesn't get any clearer than this. This is a huge, well designed study. It found that the low fat diet caused significant harm in people with diabetes by raising their blood sugars. The broader study already confirmed that the low fat diet didn't do squat to prevent heart disease in anyone who participated in the study.
Yet not a word about this study made it into any major newspaper. I only found this study thanks to an alert reader who posted the link in the comments section of the previous post.
Is this shameful? Yes. Typical. Yes. Tragic for the millions of people with diabetes who get their health information, such as it is, from mainstream media. You tell me . . .
Only by reading the full article do we learn that the researchers concluded this after an undisclosed, but probably low, number of "obesity-resistant rats" were "fed... either a high-fat or a control diet from the first day of gestation."
Rodents have evolved to eat a very different diet than humans and don't do well on high fat diets. They have very different pancreases and enzyme function than humans. And, of course, the "high fat diet" used in rat research is also a high carbohydrate diet. But that didn't deter the media from reporting this finding as if it were a human study.
Another study that was reported in the media claimed that "Pregnant women who tuck into fatty foods are at greater risk of having a stillbirth."
Further reading reveals that "The team studied two dozen pregnant Japanese macaque monkeys, an animal that has a placental structure similar to humans." Not mentioned here is the fact that Macaques, like other monkeys, have evolved to eat a very different diet from humans. They live mostly on fruits, herbs, and seeds, seasoned with the occasional insect, and can't tolerate the diet of fatty meat that humans evolved to not only tolerate but flourish on.
These are just a few of the animal research studies demonizing the impact of fat on females that appeared over the past month. But what about research that looked at the impact of fatty diets on female humans?
There was , it turns out, a blockbuster human study published this past month--an important study that described the impact of a low fat diet on real, live human women. Shockingly, it received no mention in the press at all.
But what a study it was! Unlike the studies that featured a dozen monkeys or a lab full of rats, this study tracked the outcomes for 2,263 human women, whose diet, blood sugar, and insulin were tracked for six full years.
And what it found was this: Low fat diets harm women with diabetes. Here's the study:
Effects of a low-fat dietary intervention on glucose, insulin, and insulin resistance in the Women's Health Initiative (WHI) Dietary Modification trial Shikany JM, et al. Am J Clin Nutr. 2011 May 11. [Epub ahead of print]
To understand how important a result this was, we need to back track a little and remind ourselves of what the largest and best designed study of the low fat diet has already proven, which is that in almost 49,000 middle aged women, tracked over eight years, the low fat diet was shown to have zero effect on preventing heart disease or stroke. None. Nada. Zip.
The earlier publication describing the WHI findings concluded
Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women.You can find the report from that study here:
Low-Fat Dietary Pattern and Risk of Cardiovascular Disease:The Women's Health Initiative Randomized Controlled Dietary Modification Trial Barbara V. Howard et al. JAMAVol. 295 No. 6, February 8, 2006
When this result hit the press in 2006, the media and the high profile doctors who have been promoting the low fat diet for decades responded by asserting that the diet used in the study must not have been low enough in fat, or that the study hadn't lasted long enough to demonstrate the benefits that the low fat diet must have. No one was willing to admit that maybe the study had proven what it looked like it proved--that the low fat diet was a useless intervention.
Doctors continue to recommend low fat diets. Dietitians continue to warn people with diabetes about the dangers of eating fat.
But now, this lastest analysis of the WHI data shows just how wrong-headed they are, because what the researches did here is to take the further step of analyzing the results for the subset of women for whom they had blood sugar measurements at the start of the study.
What they found was that for women with diabetes, the low fat diet wasn't just useless, it was dangerous, because it raised their blood sugar significantly--and I don't mean just statistically significantly. I mean it raised it a lot.
In the study's words, "...diabetic women had an increase in glucose that was 7.9 ± 20.3 mg/dL greater in the DM [diabetes]-I[ntervention, i.e. low fat diet group] than in the DM-C[ontrol] group (P for interaction <0.001).
In short, women with diabetes who didn't eat a low fat diet ended up with much better blood sugars, even though both groups were eating a high carbohydrate diet!
Since these were diabetic women who were likely to be taking medications to lower their blood sugar, the rise in blood sugar seen on the low fat diet is worse than it looks, because it takes into account the higher doses of medications they were probably taking.
Science doesn't get any clearer than this. This is a huge, well designed study. It found that the low fat diet caused significant harm in people with diabetes by raising their blood sugars. The broader study already confirmed that the low fat diet didn't do squat to prevent heart disease in anyone who participated in the study.
Yet not a word about this study made it into any major newspaper. I only found this study thanks to an alert reader who posted the link in the comments section of the previous post.
Is this shameful? Yes. Typical. Yes. Tragic for the millions of people with diabetes who get their health information, such as it is, from mainstream media. You tell me . . .
Subscribe to:
Posts (Atom)