Diabetes Update

Yet Another Drug Study Shows Lowering LDL Does Not Affect Clogging of Arteries

2008-05-07T07:58:00.005-04:00

The proposition that lowering LDL with drugs will protect you against developing clogged arteries just took another body blow.

We already saw that lowering LDL with Zetia and Vytorin did not lead to any improvement in the thickening in artery walls, and may, in fact, have actually worsened it in the case of Vytorin.

Now a 5 year study of fenofibrate, another drug that lowers LDL dramatically, has found the same thing. People who took it saw their LDL decline, but their arterial walls continued to thicken.

You can read about the presentation that described this finding in a report on HERE It was published in Diabetes in Control.

It's time to face the fact that the only reason doctors believe that lowering LDL is protective against heart disease is that the statin manufacturers sold their drugs for years on that premise.

But subsequent research is showing that the only reason that the statins seem to slightly lower the incidence of heart attack in middle aged men with pre-existing heart disease is because they fight inflammation. Studies reveal that statins do not prevent heart disease in women nor in men not already diagnosed with heart disease.

So as study after study finds that lowering LDL has no effect on how clogged arteries get, it is starting to look very clear that lowering your LDL is not going to prevent arterial thickening.

This is an issue of major concern to people with abnormal blood sugar now that we have learned that statins increase insulin resistance. There is also accumulating evidence that statins may promote cancer in older people. You can find the research cites that back up those findings that by visiting my web page about Dangerous Drugs for People with Diabetes.

So if these drugs won't prevent artery clogging, what will? Well, if you have been reading this blog for a while, you probably know my answer:

1. Maintain normal blood sugar levels.

2. Achieve normal blood sugars using the strategies that minimize the amount of insulin in your system. Insulin is a growth hormone and too much of it may grow the lining of your arteries.

3. The best way to do this is to cut back on your carb intake until you are getting normal blood sugars after meals. Avoid drugs like glyburide, amaryl, Prandin, and Starlix that lower blood sugar stimulating insulin production and use instead metformin which lowers blood sugar by decreasing insulin resistance.

Another study published in this week's Diabetes in Control newsletter found that metformin had a much more positive effect on the cardiovascular system than did Prandin even when blood sugars achieved were the same.

A Lesson from People with Lyme Disease

2008-05-05T08:42:00.010-04:00

There was an interesting story in the news last week about how people with Lyme Disease organized and brought so much legal pressure on the Infections Disease Society--the organization that provides treatment guidelines for infectious disease--that the IDS was forced to agree to reconsider the recommendations it puts out for the diagnosis and treatment of Lyme Disease.

You can read about it here: Doctors to Reassess Antibiotics for 'Chronic Lyme Disease'.

The background on this story is that the doctors who make up the IDS have continued to deny that there is such a thing as Chronic Lyme Disease or that it should be treated with aggressive antibiotic campaigns despite the experience of many sufferers from Lyme Disease who have developed long term disease syndromes that responded dramatically to the antibiotic treatment.

Because the official treatment guidelines claim that chronic Lyme Disease does not exist and discourage antibiotic treatment for it, people with Lyme Disease cannot get insurance coverage for their treatments, to say nothing of being unable to get their doctors to prescribe the drugs that other people with Lyme Disease have found so helpful.

Does this remind you of anything we people with diabetes go through? Like, perhaps, the way that the American Diabetes Association--a wholly owned subsidiary of Big Pharma and the large junk food companies--has taken to itself the role of defining not only the diagnostic criteria for diabetes but also the blood sugar targets doctors are told to recommend as well as what the drugs and dietary approaches those doctors should prescribe?

The ADA's criteria and treatment recommendations hurt every single person with diabetes, but because they are the official treatment standards, no doctor can be sued for following them.

Let's review exactly what is wrong with the ADA's many positions on Diabetes:

1. The ADA's Diagnostic Criteria were set intentionally high so that people with Type 2 diabetes are not diagnosed until very late in the disease process, right before they are likely to develop retinopathy. That is why more than 1/2 of all people with Type 2 diabetes have a serious diabetic complication--usually neuropathy (nerve pain)--on the day of diagnosis, despite the fact that we know it takes about ten years of exposure to high blood sugars for neuropathy to develop.

The ADA has fought very hard against any revision of its diagnostic criteria, though study after study shows that truly normal blood sugars are much lower than the range that the ADA defines as "prediabetic." The fasting blood sugar test that the ADA tells doctors to use for screening for diabetes also is known to miss full fledged diabetes in women and people of color who usually develop extremely high blood sugars after meals long before their fasting blood sugar deteriorates. This is documented in great detail here: Misdiagnosis by Design the Story Behind the ADA Diagnostic Criteria.

2. The ADA's Blood Sugar Targets for People with Diabetes which are the one most family doctors still follow are set so high that a person with Type 2 who follows them almost guarantees that they will develop complications. Despite a load of peer-reviewed evidence that blood sugars over 140 mg/dl (7.7 mmol/L) are associated with the development of retinopathy and neuropathy, the ADA still tells doctors that a blood sugar of 180 mg/dl (10 mmol/L) two hours after a meal is "tight control" and that an A1c of 7% which represents an average blood sugar well over 140 at all times is "Excellent."

It isn't, but the ADA has refused to lower its blood sugar targets, possibly because the drugs that its financial sponsors sell are not capable of lowering the blood sugar of the typical Type 2 below those very high levels. To do that, a person with Type 2 Diabetes must also cut carbohydrates. If they do that, they can usually achieve normal blood sugars. Which brings us to the third and most damning failure of the ADA:

3. The ADA Actively Promotes the Consumption of Very High Carbohydrate Diets despite decades of evidence that these diets harm people with diabetes. You need only look at the recipes in an ADA magazine for people with Diabetes to see that the ADA is still promoting the idea that people with diabetes need to eat high carbohydrate fruits like bananas and apples along with high carbohydrate pastas and grains. The ADA partnered with Campbell Soups--a company whose high carbohydrate foods are notorious for their unnecessarily high levels of sodium and high fructose corn syrup. The ADA tells people with diabetes that they should eat sugar--possibly as a sop to their other huge contributor, Cadbury Scweppes, the candy maker.

And though it's main mission is "education" the ADA does not mention anywhere in its educational materials that it is carbohydrates that raise blood sugar and that by lowering carbohydrate intake, people with diabetes can restore their blood sugar control. Instead, the ADA tells people with diabetes to eat high carb diets and then take every single one of the drugs its Big Pharma sponsors sell, including Avandia, which the ADA went out of its way to urge patients to continue to take after the data came out showing it increased the likelihood of heart attack.

4. The millions of dollars that pour into ADA coffers thanks to its aggressive fundraising do not fund diabetes research. The ADA's primary mission is solely "education." The one thing that the ADA does re research is to publish two medical journals, Diabetes and Diabetes Care, which publish research--much of it funded by its drug company sponsors. However, if you price a subscription to either of these magazines, you will see that these journals are a profit center for the ADA. They are expensive! And the ADA's leadership usually ignores the results of the research published in those journals when setting treatment guidelines.

Much of the money you hard working people with diabetes raise with bake sales and other community activities funds the enormous salaries of the ADA's top executives, who are people who come from backgrounds as health industry lobbyists or from heading other disease charities completely unrelated to diabetes. The ADA's leadership do not have diabetes themselves, and have been known to refer to us folks who do as "poor victims."

Well, we are poor victims as long as we let these health industry profiteers earn huge salaries for fighting AGAINST us people with diabetes getting timely diagnoses, while refusing to teach physicians the safe blood sugar target recommendations that could keep us from developing complications, and actively campaigning against giving people with diabetes accurate dietary advice.

It is time we looked into how the people with Lyme Disease got some action from the organization that has a stranglehold on the treatment for their health condition and got into doing some organizing of our own.

The damage being done by the ADA to people with diabetes is far, far worse than anything the Lyme Disease people have to contend with!

Type What?

2008-05-02T11:10:00.004-04:00

A study published in the most recent edition of the journal Diabetes makes it even more clear that the usual division of diabetes into "Type 1" and "Type 2" is an oversimplification.

The usual mythology has it that Type 1 is an autoimmune disease and people who get it are innocent bystanders while Type 2 is caused by overindulgence and people who get it should be ashamed of themselves.

I've written at length about why the second part of this formula is bull crud. You can read the many reasons HERE.

But there is no question that framing the diagnosis of diabetes this way has made many people with autoimmune forms of diabetes hostile to those with Type 2, because they feel that an ignorant public unfairly blames them for causing their condition and believe, with the rest of that ignorant public that those gluttonous lazy type 2s do deserve such blame.

But the latest research on LADA, the adult onset form of autoimmune diabetes, has come up with a finding that makes it clear how wrong this kind of thinking is. The researchers in this study, which you can find at the Diabetes web site:

Autoimmune Diabetes in Adults, Type 1 Diabetes, and Type 2 Diabetes

examined the genes of 361 peole with LADA, 718 people with type 1 diabetes, and 1,676 type 2 diabetic patients, as well as 1,704 healthy control subjects from Sweden and Finland.

They found that "LADA subjects showed, compared with type 2 diabetic patients, increased frequency of risk for the HLA-DQB1 *0201/*0302 genotype with similar frequency as with type 1 diabetes (36%)." There were some other similarites with Type 1, genetically, but then they also found that "the frequency of the type 2 diabetes–associated CT/TT genotypes of rs7903146 in the TCF7L2 were increased in LADA subjects (52.8%; P = 0.03), to the same extent as in type 2 diabetic subjects (54.1%, P = 3 x 10–7), compared with control subjects (44.8%) and type 1 diabetic subjects (43.3%).

In short, these LADAs had both type 1 genes--autoimmune genes--AND type 2 genes.

This finding is particularly interesting in light of an earlier finding that slightly under 10% of people diagnosed with Type 2 also have autoimmune markers like elevated GAD antibodies.

TCF7L2 is one of the more common defective genes found in Type 2 diabetes but by no means the only one. HNF4-a is another gene that has been found in association with both a form of MODY and with a Type 2 diabetes in both Ashkenazi Jewish and Danish populations.

In addition, as they get older, many Type 1s find their insulin needs rise, as they become insulin resistant and probably start expressing the Type 2 genes they inherited. Doctors do not give Type 1s who are using larger doses of insulin metformin, but my guess is that they probably should. I'm not very insulin resistant at all--two or three units is all it takes to drop my blood sugar dramatically, but even so, I can drop my insulin needs by about 1/3 by taking metformin. But here again, the division of diabetes into these two artificial types is hurting people because doctors do not think that a "Type 1" might also have the genes that in middle age would have expressed as "Type 2" had they not also suffered an autoimmune attack.

So it is time we dispensed with the artificial division of diabetes into Type 1 and Type 2. Let's admit that "Diabetes" is really nothing more than a symptom--high blood sugar--and that the causes of that symptom are many and not mutually exclusive.

When the damage is to the immune system, we get autoimmune attack on the beta cells. When the damage is to the genes that regulate insulin resistance in the muscles--and possibly mitochondrial function, we get another form of diabetes, when the damage is to the genes that regulate the beta cell's response to rising glucose levels in the blood we get secretory defects, when the body suffers genetic damage thanks to exposure to chemicals in the environment we get yet more blood sugar abnormalities, and like the unlucky LADAs, some of us get more than one of these problems going on at once.

And those of us who do have abnormal glucose metabolism should resist the temptation to divide people with diabetes into types and to use this typology to define some of us as blameless and others as blamable diabetics.

That kind of division helps no one. All of us should be putting our efforts into ensuring that EVERY person with diabetes gets the kind of excellent, health-preserving treatment that so few of us currently get from the doctors, nutritionists, and drug companies who see us as little more than a huge profit center.

More Evidence Scary Chemicals are In our Bodies

2008-05-01T17:01:00.005-04:00

Science Daily today reported on a recent study that found both Teflon and Scotchgard in the milk of nursing mothers. The study turned out to have been done by a wonderful woman scientist I have the privilege of knowing personally, but that wasn't why I clicked through on the headline. It looked like yet another study, like those on plastics and pesticides, which point to hidden causes of the so-called "diabetes epidemic."

Suspected Carcinogenic Chemicals Used To Make Teflon, Scotchgard, Found In Human Milk

If this doesn't scare you, you don't understand much about physiology.

It scares me plenty, not just because these are carcinogens, but because this is yet more proof of the extent to which bizarre, not-found-in-nature, chemicals that are added to food packaging get into our bodies where no one really has much idea of what they do.

The other scary thing about this particular bunch of chemicals is that they don't break down once they are in the body. So whatever the "safe" level might be over time, you are getting more and more of them over time and they are probably being deposited in random places throughout your organs.

These ubiquitous chemicals like bisphenol-A and pesticides may also raise the incidence of diabetes and increase insulin resistance. Things that cause cancer often do.

Many people attribute the diabetes "epidemic" to the huge surge in obesity. There is no doubt that the incidence of obesity has greatly increased, but what people don't understand is that obesity is often the result of genetic damage caused by environmental toxins. In fact, lab scientists usually interpret obesity in animals as a sign that they have experienced genetic damage. A healthy animal won't overeat, but those with genetic damage do.

Note that the article mentions that "Food sources of PFCs [Perfluorinated compounds] include grease-resistant packaging such as microwave popcorn bags and pizza boxes, as well as fish and other animals that contain these chemicals. Exposure can also come from personal care products including dental floss and shampoo." And of course, your nonstick cookware is coated with Teflon and it leaches into food, especially when you heat it a bit too much.

Whaddya know? You've Already Cured Your Diabetes!

2008-04-25T08:40:00.008-04:00

Frank who posts as "Jefferson" on alt.support.diabetes, posted the description of the clinical trial now underway to test whether gastric bypass cures Type 2 diabetes in people as well as in mice.

Here is the protocol from the NIH Clinical Trials web site:
Study of Duodenal-Jejunal Bypass as a Potential Cure for Type 2 Diabetes Mellitus

What immediately leaps out of the description of the protocol is this statement:

The clinical resolution of T2DM is defined as independence of all anti-diabetic medications and maintaining a HbA1c less than 6.0.

This should raise huge red flags in all of us, because by this definition all of the many hundreds of members of the 5% Club who have lowered their A1cs by cutting down on their carbs have already "cured" their diabetes. You can read reports from members of the 5% Club HERE.

I immediately ask myself, why didn't 60 Minutes run a story about how cutting back on carbs can "cure diabetes?"

But of course, no one makes $25,000 selling low carb diets to people with diabetes, while that is the usual tab for Gastric Bypass surgery.

And as all of us who have lowered our A1cs to the normal range know very well, Diabetes is not "cured" when you lower your A1c to 5.9%. You've cut way down on your chances of developing complications, but the underlying problem still remains. And whether attaining the lower A1cs by crippling your digestive system will produce permanent normal blood sugars in people for whom the bypass does not cause permanent malnutrition syndrome is very questionable.

When gastric bypass is successful for weight loss and does not produce complications that destroy the gut and produce malnutrition syndromes it often works onlyfor a few years and then fails--often leading to weight regain.

So for all of those who have been hailing this radical surgery as a cure for diabetes there already IS a "cure" for diabetes that does not require you to risk your life. It's called carbohydrate restriction and it works very well.

To learn how to "cure" your diabetes follow the technique explained here:

http://alt-support-diabetes.org/newlydiagnosed.htm

(Note: The Jennifer who wrote this wonderful advice is another person, not me!)

Study Shows Benefits of Exercise on Diabetes are Minimal

2008-04-23T13:48:00.006-04:00

An article cited in the medical news recently states "...the prescription of group-based brisk walking represents an equally effective interventional strategy to modulate glycaemic control and cardiovascular risk profile in type 2 diabetes patients compared with a more individualised medical fitness programme."

Sounds good, eh?

But let's look at what they really found.

The study is here: Brisk walking compared with an individualised medical fitness programme for patients with type 2 diabetes: a randomised controlled trial. S. F. E. Praet et. al. Diabetologia, 10.1007/s00125-008-0950-y.

The researchers took 100 people with diabetes and put half of them on a brisk walking regimen that included some resistance exercises. They put the other half on a traditional gym regimen that used machines like elliptical trainers and emphasized weight lifting.

At the end of the year they measured the improvement of the 37 people who stuck with the program.

Thirty seven? Out of one hundred. Hmmm. That's only a tad more than 1/3. In fact, several people recruited dropped out at the very start of the study so only 92 began the exercise programs. So far, this study sounds a lot like real life to me.

But since some did stick with it, let's look at how effective these exercise programs were for blood sugar control.

For all participants, the mean A1c dropped by .14%. That translates out to a lowering of average blood sugar of 4 mg/dl--which is underwhelming when you learn that the beginning average A1c was 7.13% ± 1.36.

The group that did brisk walking dropped their average A1c by .11 and the traditional gym program folks by .18. Hmmm again. That equates to something like 3 mg/dl or 5 mg/dl. It is starting to look like they could have achieved a much better lowering of A1c by dropping 15 grams of carbs from their daily intake.

Their fasting blood sugar declined about 4 mg/dl--in a group that started with a fasting blood sugar that averaged 152 mg/dl.

But surely there must have been other benefits? What about weight? Gyms sell their programs as being a major route to weight loss. Well, that wasn't much better. The people doing the brisk walking lost on average .2% of their BMI. (The researchers did not give the actual amount of weight lost.)

At my BMI, .2% computes to a loss of 1 lb. Over an entire year. The gym group did only slightly better. They lost an average of .8% of their BMI. That is about 4 lbs.

The rest of the parameters they measured weren't much better. Systolic blood pressure decreased about 10 mmhg. Diastolic (the bottom number) by about 5 mmhg. Cholesterol decreased by a similar trivial amount.

I'm scratching my head. Did the researchers really call this an "effective interventional strategy to modulate glycaemic control and cardiovascular risk profile in type 2 diabetes patients?"

Would any sane person put themselves through all the effort of doing all that exercise if they knew in advance that their results would be so unimpressive?

I like walking. It does good things for my leg muscles and makes me feel healthier, but having read this study I feel a lot better about my own results which, over the years, have been no weight loss, and no change in blood pressure or blood sugar no matter how long or regularly I walked.

I thought I was some kind of oddball, but these results suggest I am in fact typical.

But you do have to wonder who comes up with these definitions of "effective!"

More on the Actual Gastric Bypass Death Rate

2008-04-22T14:52:00.006-04:00

A helpful blog reader send me the full PDF version of the study of the long term outcome of weight loss surgery in Pennsylvania which was cited in the previous blog post.

Death Rates and Causes of Death after Bariatric Surgery for Pennsylvania Residents 1994-2004. Bennet I. Omalu et. al. Arch Surg. 2007;142(10):923-928.

Typically when a surgeon tells you the mortality rate for a surgery, he tells you only the percentage of those who died within 30 days of the surgery. This study looked both at the actual deaths within 30 days after surgery and in the death rate in the years after the surgery.

As the study reports, in the 16,683 people who had weight loss surgery in Pennsylvania between 1994 and 2004, .9% died within 30 days of the surgery. That translated into 150 people.

But wait. That statistic was taken from the group as a whole. When the population is broken out by age, a much scarier statistic emerges: In the age group 55-64 1.53% were dead within 30 days, or 15 out of 1000 who had the surgery. And for the age group of those 65 and older, 3.1% died within 30 days, or 3 out of every hundred.

But that was just in the first 30 days after surgery. The study looked at time since surgery, and with each passing year the number of dead grew greater.

By one year after surgery, 2.1% of the group had died. (Twenty-one out of every thousand.) By two years, 2.9%. Then things got worse. Three years after they had had the surgery, 3.7% were dead. By four years, 4.8% and by five years, 6.4%.

The authors of this study remark that they did not follow up on the results of subsequent surgeries. But other studies have found that many people who have weight loss surgery require one or more follow up surgeries in the years that follow the initial surgery. It is likely that each subsequent surgery raises the risk of further complications and death.

Another chilling statistic emerged from the analysis of this data. In a population of the same size of the same demographic make up, the expected number of suicides would be 2. However, in this group, there were 16 suicides and an additional 14 drug overdose deaths. Most of these occurred at least one year after the surgery. The authors of the study speculate that many of the drug overdoses were probably suicides too, and flag this as a serious problem that requires more study.

What was missing in this study was one important piece of information: the weight loss achieved by the people who died. The authors assume that the high death rate is due to health conditions contracted while obese or due to weight regain. But this is only speculation. They did not review any statistics about the size of the people at death, which would have been difficult to do since only about 1/3 of these victims were autopsied.

But based on stories I have heard and cases like Mrs. Yamin's it may be premature to assume that the deaths were caused by obesity. Mrs. Yamin weighed 100 lbs at her death. Instead deaths may have been caused by long term malnutrition--i.e. starvation. Though the most common cause of death listed on death certificates after a year was cardiovascular (i.e. heart attacks) that is what kills a lot of people with anorexia and starvation. When the body is no longer absorbing nutrients the electrolytes can become dangerously unbalanced and that causes heart attack. Without independent autopsies, it is very hard to know what really happened.

Doctors don't like autopsies, because a patient who didn't have an autopsy is a patient whose family is going to have a much tougher time suing for malpractice. So if a heart stops beating, well, write it down as cardiovascular death, and since the person was once fat, who is going to challenge it?

But folks, please take these statistics seriously. And please note that the things that killed people within the first 30 days were NOT necessarily caused by obesity. Among the biggest killers were pulmonary embolism (20.7% of all early deaths)and sepsis (i.e. infection that spread through the body causing organ shut down). Sepsis killed 11.3% of those who died in the first 30 days. One out of four died of vaguely specified "therapeutic complications" which is a catchall term entered on the death certificate that included things like sepsis, bleeding, ruptured surgical wounds, etc.

One last word. Many people erroneously believe that before a doctor can perform a specific kind of surgery, that surgery must undergo the same kind of safety testing and approval process that drugs get. This is not true. Surgeons can perform any surgery they want, as long as they are licensed surgeons.

There is only one limitation on what kind of surgeries are performed: whether or not insurance companies will pay for them. Most insurers won't pay for operations that have a poor safety record--once they have enough data to know that the operation isn't safe.

But weight loss surgery is usually NOT paid for by insurers. Like plastic surgery, it is a surgery that patients pay for out of their own funds. This is one reason surgeons promote it so strongly. There are no forms for them to to fill out, no limit on what they can charge, and most importantly, no evaluating the patient's suitability for the surgery by pesky insurance review boards. All the doctor has to do is sell the patient on the operation, and the fun can begin.

So don't let yourself become a victim of a surgeon who has found a dandy way to make himself a multi-millionaire. And don't trust that the doctor who stands to make $25,000 for a few hours of work has your welfare in mind when he assures you that a surgery is no more dangerous than crossing the street. Remember, surgeons rarely track the outcome of their surgeries beyond six weeks. But as the Pennsylvania study suggests weight loss surgery keeps on killing for years after the initial surgery.

Don't let yourself become a victim.

Gastric Bypass Cures and Kills

2008-04-21T09:40:00.007-04:00

Yesterday night the TV news show, 60 Minutes, ran a segment promoting the idea that gastric bypass surgery can cure diabetes. Not content with promoting this dangerous surgery to the morbidly obese, surgeons are now recommending it for people who are merely overweight.

This is scary.

Why? Because this surgery kills people. Doctors promote it for the morbidly obese by claiming that their weight will kill them anyway. What they don't point out, is that the surgery can kill them a lot faster than their weight will. Something like 1 in 200 people who have gastric bypass surgery die within six weeks of the surgery.

But what is far more significant is that many more people who have this surgery--including those who lose a lot of weight--die within five years of the surgery.

Unfortunately, the way that surgeons collect data about the success of their surgeries ensures that the public does not learn these statistics. Doctors claim that the surgery is no more dangerous than gall bladder surgery, but this is only true if you look at the statistics collected within a few weeks of the surgery. But unlike gall bladder surgery, once the surgery heals the complications have only begun.

The Junkfood Science blog alertly reported on a study that tracked long term mortality after weight loss surgery. That study is found HERE but the full article is pay only so we have to rely on the blog authors for the details.

What Junkfood Science reports is that this study found this: "We also estimated the long-term mortality for individuals who had undergone surgery many years ago. For the 1995 cohort who had at least 9 years of follow-up, 13.0% had died. From the 1996 cohort with 8 years of follow-up, 15.8% had died, and from the 1997 cohort with 7 years of follow-up, 10.5% had died. For the 1998-1999 cohorts with 5 to 6 years of follow-up, the total mortality was 7.0% to 2004."

Junkfood Science's author then looked at death rates for people with the same demographic who did not have surgery and reports "The U.S. National Center for Health Statistics of the Centers for Disease Control and Prevention data reports that the overall death rates among Americans of the same age is 0.352% — for men it is 0.44% while for women this age it’s 0.26%."

So basically people who had weight loss surgery were dying at a rate many times higher than normal--even the rate normal for obese people.

All this is abstract and statistical until we start putting a face on some of the victims who did not make it into the mortality statistics because their deaths--though caused by the complications of weight loss surgery--took five or more years to occur. One of them turns out to be Claudette Yamin, the much-beloved mother of Elliott Yamin, the American Idol finalist who uses in insulin pump to control his Type 1 diabetes.

Many of us fell in love with "Mama Yamin" as she qvelled with happiness at her son's unexpected success. What we didn't know when we saw her hobbling through the crowds was that she had undergone dozens of operations for the complications of the weight loss surgery she had undergone five years ago and was periodically hospitalized for protein supplementation because she was starving to death. This past month the complications killed her. She died rail thin, at 65 years old, still full of vitality and enthusiasm for life.

She spoke about her complications from weight loss surgery on this television interview: http://www.youtube.com/watch?v=28JEjVK6dnw

As you can see in the interview, Claudette Yamin was told that her anorexia after surgery was an emotional problem. In fact, it probably was not. The incidence of severe psychiatric problems after such surgery is surprisingly high, as documented by Bama Gal in the Back Across the Line blog. Because the surgery changes the functioning of incretin hormones which are known to affect how the brain relates to food, the anorexia that is caused by this surgery is most likely physiological in nature.

I personally have experienced how powerful the manipulation of incretin hormones can be in affecting the hunger response when I became anorexic after two months on Januvia. The anorexia vanished when I stopped taking the drug, but while I did it became harder and harder to eat anything, which for me, food lover that I am, was bizarrely odd. But for the last month while the drug was in my system it was as if food no longer was food, but plastic. Eating became a weird experience as it seemed odd to put this stuff into my body.

Gastric surgery permanently changes how incretin hormones work--which is probably why it can "cure" diabetes in some people, since incretin hormones are deeply involved in the secretion of both insulin and glucagon. But the anorexia when it occurs does NOT go away and as we all know, anorexia kills.

The other way that weight loss surgery kills, long term is by destroying the stomach's ability to absorb nutrients from food. Though some forms of weight loss surgery are supposed to be reversible, this is not always true. Bands can grow into the stomach and cannot be removed. Wounds in the stomach may not heal and may end up destroying stomach tissue permanently. And once the stomach tissue is destroyed, you may fall victim to relentless malnutrition syndromes because your body can no longer absorb nutrients from your food no matter what you eat. Then it is time for visits to the hospital for intravenous supplementation. For the rest of your life.

At that point, the fact that you "cured" your diabetes may be a wry triumph, since you are basically starving to death.

So before you let some knife happy surgeon--who only follows his patients for six weeks after surgery--talk you into what might be a fatal cure for your diabetes, try some of the other strategies that will control your diabetes and help you lose weight without risking your life.

1. Cut the carbs. It appalls me that this dangerous, irreversible weight loss surgery is being promoted as safe by the the same doctors and organizations who continue to warn people with diabetes that "low carb dieting might be dangerous" despite the fact that a decade of research has not yet uncovered any evidence that low carbing does anything but lower blood sugar and improve lipids.

2. Try Byetta for weight loss. The anorexia induced by Byetta is reversible and it doesn't appear to do anything permanent to your stomach and intestines. For some people it can lead to dramatic weight loss. It is worth a try. For many people with diabetes Byetta is much more effective for hunger control than it is blood sugar control so if you use Byetta, keep an eye on your blood sugars and if they are too high, make sure you have other strategies in place to control the blood sugars while you limit appetite.

3. If you are on insulin, ask your doctor about Symlin. It may also have weight loss benefits for some people.

4. Ask yourself: Is it worth "curing" your diabetes by having a surgery that gives you a 1 in 6 chance of being dead in 10 years? The reality is that it takes 20-30 years of extremely poorly controlled diabetes to kill most people. And if you control your blood sugar which most of us can do very well and keep your A1c in the 5% range you will live much, much longer than that, complication free. Being thin might be nice, but the fact is all of us know obese people who have lived long and productive lives while tipping the scales at 300 lbs for decades. I certainly have. Perhaps there is nothing right now that will get the weight off you, but you can still control your blood sugar, and there is always the possibility that in time some new finding will lead to a medication that will be effective for you.

It's worth staying alive to find out. Even if you have to put some effort into controlling your blood sugars.

Statins make you fat and insulin resistant?

2008-04-19T10:00:00.003-04:00

Among the studies you did not see highlighted in the media recently was this study published in the journal Diabetes Care:

Simvastatin Improves Flow-Mediated Dilation but Reduces Adiponectin Levels and Insulin Sensitivity in Hypercholesterolemic Patients

The reason is that the big drug companies do not put their publicity machine behind studies that call into question the safety or healthfulness of their blockbuster drugs. And that is exactly what this study did.

Simvastatin is Zocor. What this small but interesting study found was that "Simvastatin significantly improved endothelium-dependent dilation, but reduced adiponectin levels and insulin sensitivity in hypercholesterolemic patients independent of dose and the extent of apolipoprotein B reduction."

Translated into English this means that Zocor reduced cholesterol and improved the elasticity of arteries, but did this at the cost of increasing insulin resistance and decreasing the hormone, adiponectin, that keeps people from gaining weight.

Can this be yet another reason for the so-called "Diabetes Epidemic?" It would be ironic if the overprescribing of statins to people with mildly elevated cholesterol turns out to be a major factor in worsening blood sugars.

We know that giving statins to people who don't already have heart disease does very little to improve health. But we also know that raising blood sugar by the amount needed to raise A1c by as little as 1% (i.e. from 4.7% to 5.7%) is enough to create a very significant increase in heart attack risk.

Hmmmmm. . . . .

The Four Fast Acting Insulins Have Different Activity Curves

2008-04-18T11:21:00.006-04:00

Fasting acting insulin is the insulin you inject to cover the rise in your blood sugar that occurs after you eat a meal.

They are called "fast acting" because unlike the basal insulins, Lantus and Levemir, they are absorbed relatively quickly after injection. This is what makes it possible to use these fast acting insulins to cover a meal.

In theory, if you can figure out how many grams of carbohydrate one unit of fast acting insulin will cover, and if you can figure out how to estimate the number of grams of carbohydrate on your plate, you can match the insulin to the meal and get normal blood sugars.

In practice this is harder than it sounds. It's tough to figure out how many grams of carb one unit will cover, especially since this amount may be different at different times of day. It is also hard to estimate how many grams of carbohydrate are actually on your plate. We'll discuss both these issues in some future blog posting.

What I want to discuss here is the speed and duration with which each of the fast acting insulins acts. This is what is called its "Activity Curve." The most important qualities of the activity curve are:

1. When the insulin reaches its fullest strength. This is also known as when the insulin "peaks." Ideally you would like the insulin to peak at the time when the carbohydrates from your meal hit your blood stream. That way most of the insulin meets most of the carbs.

2. How long the insulin stays active. Because insulin is being absorbed from the subcutaneous fat into which you injected it, it isn't all absorbed at once, so it typically takes anywhere from three to eight hours for the complete dose of a fast acting insulin to be used up.

When you get a vial or pen full of insulin, it will usually include the Prescribing Information for the insulin and that prescribing information will included a set of graphs that purport to show the activity curve for that particular insulin when used by people with Type 1 and by people with Type 2 diabetes.

What the insert does NOT tell you is that the curve you see is the average activity curve for the insulin. In fact, each of us will have our own unique response to each of the insulins and these responses can be quite different from what you see on that graph in the Prescribing Information.

Our own unique activity curve will vary depending on how large a dose we inject, how much fat we have, how much scar tissue we have at injection sites, and unique features of our metabolism that are not yet understood.

What this means in practice is that a fast acting insulin that works very well for you may work poorly for me--and vice versa. Whether a specific fast acting insulin will work well for you is something you can only determine by testing it out.

I've used all four of the fast acting insulins and while I could report on how they work for me, I won't, because my personal response to the insulin is not going to tell you much about what your response might be. Instead I'll just summarize a bit about each of the insulins so that if you want to explore using one with your doctor you'll have an idea of the range of experiences people have with these insulins.

1. Regular Human Insulin. Sold under the brand names Humulin R and Novalin R this insulin has the identical make up to the stuff your body makes. Because your body dumps this kind of insulin right into your circulatory system, it isn't designed to be absorbed from fat and thus when injected it absorbs into the blood stream relatively slowly. This is not necessarily a bad thing.

Most people report that they must inject R insulin from between 45 minutes to 1 hour before eating and that it stays active for the next 4-8 hours, depending on the size of the dose. The bigger the dose, the longer it stays active. However it usually peaks between 2 and 3 hours after injection and when used in small doses (5 units e.g.) it is usually finished acting by five hours. If you are eating a fairly low carb diet or one rich in fibrous, slow-digesting carbohydrates, this may a very good insulin to use because its long slow curve is more likely to match the pattern of your rising blood sugar after a meal.

R is also a very good insulin for people who are prone to hypo, because it is much slower in its action so you get more of a warning period as blood sugars drop before you go really low. Because of its slower speed--it may stay active for up to 8 hours, it may have a bit of a residual effect that will lower fasting blood sugar the next day. This is not true of any of the other, faster, insulins.

The final advantage of R is that it is much, much cheaper than the other insulins we'll discuss. You can buy it at Wal-Mart for about $22 a vial. Everywhere else it is about $36 a vial. You do not need a prescription to buy R insulin (though you may need one for the needles.)

2. Humalog. This is Lilly's fast acting insulin and it is the one that most people seem to start out using when their doctors prescribe fast acting insulin. Many people find that Humalog works well if they inject no more than 15 minutes before eating. Some can inject it right before eating.

Humalog should peak about 1 hour after injection and it is supposed to stay active for about three hours. Dr. Bernstein says that you should use 1/3 less of a dose of Humalog than you would use for R. Though many people find this the ideal insulin to use, a few report that it causes a pattern of highs at one hour followed by lows at three hours when they inject it as directed.

3. Novolog. This is Novo-Nordisk's fast acting insulin. If you are having problems with Humalog, it is well worth a try. Novolog is also injected no more than 15 minutes before eating and it peaks one hour after injection. It too should be done by 3 hours. It can be dosed identically to R insulin.

4. Apidra.This is Sanofi-Aventis's fast acting insulin. It is the newest of the fast acting insulins. It is a bit faster than either Humalog or Novolog and many people (self included) find it can be injected at the time of eating or even after eating and work very well. However, it also clears out of the body faster than the other insulins, which can mean that if you have slower digesting carbohydrates in your meal, the insulin my be finished before the carbs get into your blood stream. If this is an issue, you can split your doses and use two shots if you have eaten something like Pizza that you know will cause a delayed spike.

Apidra is not available yet in the U.S. in a disposable pen, though a version in the Solostar disposable pen is currently available in Europe. In the U.S. it currently comes in either a vial or cartridges which you can use with the Opticlik pen. The problem with this pen is that you can only get it from your doctor, so if you lose it or it goes bad on a weekend or when your doctor doesn't have any more, you can be SOL. Plus it is enormous.

Changes in Your Response to a Specific Insulin. After using fast acting insulin for several years, I've learned that my body's response to a particular insulin may change over time. It may work very well for a while and then the timing will start to change. There are several reasons for this:

1. Insulin can go bad. If you are carrying around a pen in your purse in the summer, for example, the heat can kill the insulin or if the exposure is borderline, weaken it. So can a lot of bouncing around. Leaving it in a car too long can also weaken it. You can also kill insulin by putting it in the butter compartment of your fridge door if the door is full of stuff that jiggles when you open and shut the door. Insulin does not like being vibrated. Finally if your fridge is too cold, it can freeze your insulin.

2. You can develop antibodies. Injecting things into your skin is a great way to get your immune system riled up, and over time many of us develop antibodies that attack the insulin proteins we inject. This can make the insulin behave unpredictably. Sometimes all you need to do is to switch to a different kind of fast acting insulin. Alternatively, you may have to use more and change the timing.

3. Random Factors. Your activity level, the temperature outside, infection, etc can all change how your body responds to a specific fast acting insulin.

If there is one thing I've learned using insulin these past couple years it is that any time I get things set up just right, something changes. This is probably the toughest part of using insulin. The books make it sound pretty cut and dried, and there is a certain amount that you learn that doesn't change, but using insulin to get normal blood sugars requires an ongoing process of continual small adjustments.

What Dose to Use?

I include this question here because I see people posting it all over the internet. The answer is "The one that is right for you." And figuring that out can take time. The dose of fast acting insulin that will cover 20 grams of carbohydrate may range from 1 unit to 20 units. It depends on how insulin resistant you are. That is something you can only learn by starting with a very low dose and slowly raising it until you see an impact.

And to answer the other question I get asked a lot, No. It is not possible to estimate how insulin resistant you are from any lab test, no matter what the doctors tell you. Nor does your weight tell how insulin resistant you are either. You'll just have to inject a very small dose of insulin when eating a meal containing a known amount of carbohydrate and see what happens next, and work up from there.

Should You be Eating the DASH Diet?

2008-04-16T09:43:00.006-04:00

This week the medical news has been highlighting the findings of the Nurses Health Study that women eating the so-called DASH diet over a period of 24 years had fewer heart attacks and strokes.

As described by press coverage the DASH diet is one that "included plenty of fruits, vegetables, nuts, legumes, and whole grains and consumption of low-fat dairy products in quantities close to the recommended dietary guidelines." The DASH diet discourages the consumption of processed and red meats, sodium, and sweetened beverages.

The limitations on this study finding, are, of course, that a) diet is self-reported. People are notoriously bad at remembering or reporting what they really ate. b) The DASH diet is more expensive than the junk food diet and c) The DASH diet is really a "low fast food", "low boxed crap" diet. There are strong socioeconomic issues involved in who eats this diet, and many of the factors that make for eating the diet--like higher education, less polluted home neighborhoods, higher status in the workplace etc, also protect against heart disease and stroke. So it is, as usual, difficult to know whether the diet causes the improvement in heart disease or if eating it is a marker of the wealth, education, and status which protect against heart disease.

My guess is that it is a combination of both.

The next question is this: assuming this diet was protective against heart disease, what does it mean for people with diabetes?

Obviously, it does not mean that they should rush out and start eating a lot of whole grains. We know for certain that exposure to high post-meal blood sugars over time raises the incidence of both heart attack and stroke. (Read the details HERE)

But there are some good takeaway messages:

1. Eat lots of low carb fruits and vegetables. These low carb fruits and vegetables should be the basis of the diet of every person with diabetes. Any "low carb" diet that does not tell you to eat as much fresh low carb vegetables as possible is not a good diet. Even those of us who have very little insulin production find that leafy greens, fibrous vegetables, and berries are very kind to our blood sugar.

There is only ONE major caveat with fruits and vegetables, which is that, sadly, while eating them may protect against heart disease, the pesticides and herbicides sprayed all over crops, especially those from the Third World countries that provide winter produce, probably cause cancer. It would have been interesting to see whether those nurses who did not get heart disease in this study had a higher incidence of cancer.

Solution? Shop your local farmers market in the spring and summer and freeze stuff for winter. "Organic" produce sold in the United States, alas, may still have pesticides in them thanks to the Republican regulators' weakening of the labeling laws.

2. Cook from scratch. Processed foods are filled with corn syrup, soy, and a long list of mystery chemicals none of which occur in food you cook from scratch.

Many of you are from the generation whose mom's did not cook, and as a result you have fallen for the myth that cooking is a complex art pursued by celebrity specialists. This is utter nonsense. Cooking is not hard. It fact, it's easy.

Ignore the cooking shows where celebrity chefs make cooking look complicated. Buy yourself a basic cook book that explains cooking techniques like The Joy of Cooking, and learn how to make any of the hundreds of meals you can cook in 15 minutes, start to finish. If you have a friend who can cook, have them show you how to make a basic sauce or thicken stew. Cooking your own low carb desserts will make it possible to eat low carb without ingesting all the frankenfood chemicals found in boxed stuff. It's also cheaper, and by the way, what you end up with actually IS low carb, which is not true of much of the boxed stuff.

3. Stay away from preserved meats. This is probably the toughest for me, because I am addicted to various forms of salami. The biggest problem with processed meat probably is the very high salt content (which is part of what makes them so addictive.)

4. Avoid being an uber control freak. Because we know that high blood sugars DO cause massive amounts of harm to the body, it is easy to think that if we just ate the "right foods" we could eliminate all the other diseases known to man. It ain't true.

If you eliminate heart disease, you get to die from either cancer, emphysema, neurological deterioration, or a long list of other metabolic breakdowns many of which are very unpleasant.

Personally, when my time comes, I'd prefer a swift and fatal heart attack. But because I'd prefer to have that heart attack while still able to walk on both legs, see with both eyes, and pee without the help of complex electronic machines, I am obsessive about blood sugar control. It isn't the stuff that kills us that worries me so much as the stuff that destroys our quality of life while we are alive.

But hey folks, the simple truth is this: none of us gets out of here alive.

The Limitations of Lantus

2008-04-15T08:35:00.005-04:00

There's a common error revealed by many emails I get as well as what I see posted on discussion boards. It has to do with the failure of medical staff to explain to patients for whom Lantus is prescribed what it is that Lantus does and what it is that Lantus cannot do.

Lantus is a basal insulin. Basal insulin are slow long-acting insulins that attempt to mimic a specific function of the healthy beta cell. Normal people's beta cells secrete tiny pulses of insulin every couple minutes throughout the day and night. These pulses allow healthy cells to take in blood sugar and use it any time they need to. This slow steady release of tiny bits of insulin is called Basal Insulin Release. It is a failed basal insulin Release that Lantus attempts to replace.

But basal insulin production is a completely separate function from the much more powerful insulin release that happens when you eat foods that contain carbohydrates. That is because the influx of a large amount of carbohydrate into the digestive system stimulates two more insulin releases--first phase and second phase insulin release. These fast, large insulin releases are much more powerful than the tiny pulses of insulin produced during basal insulin release.

The problem patients run into when they are prescribed Lantus is that they do not understand that there are these different kinds of insulin release and assume that if they are injecting insulin to replace the insulin their bodies no longer make, these injections should be enough to give them normal blood sugars.

But if Lantus is what they are injecting, it will be impossible for most people with Type 2 to get normal blood sugars when they eat any significant amount of carbohydrate. Though they inject a large dose of Lantus, that Lantus will be absorbed very slowly over a period of anywhere from 22 hours to three days. So at any given moment only a very small amount of Lantus is active in the blood stream. That is why Lantus only lowers fasting blood sugar.

Though it makes sense that if you lower your fasting blood sugar, the amount your blood sugar rises after eating a meal should be lower too, in reality, no matter how low your fasting blood sugar might be, thanks to Lantus, if you eat 60 grams of carbohydrate at one time--whether it be from "healthy" whole grains or any other starchy or sugary food, your post-meal blood sugar will still rise 150-300 mg/dl.

The exact extent of that rise depends on your weight and how many beta cells remain alive. For a person who weighs 140 lbs, 2 grams of carbohydrate will raise blood sugar 10 mg/dl. For a person who weighs 280 lbs, the same 2 grams will raise blood sugar 5 mg/dl.

Whatever residual insulin secretory function your beta cells have left will limit the rise you actually see after consuming carbohydrates, but because doctors delay prescribing any kind of insulin until a person's blood sugar control has deteriorated to where most beta cells are likely to be dead, by the time a person with Type 2 diabetes starts Lantus, it's very likely those post-meal spikes caused by eating carbohydrates will be very high indeed.

But because Lantus is absorbed so very slowly and because only small amounts of insulin are active in the body at any one time, Lantus insulin will has no effect on those high post-meal spikes at all. It's too slow and too weak.

So even if a person is taking enough Lantus to get a normal fasting blood sugar level of 85 mg/dl (which most aren't), after each high carbohydrate meal their blood sugar will be soaring well above 200 or even 400 mg/dl. Blood sugars that high damage nerves, capillaries, retinas, and kidneys and cause amputation, blindness and kidney failure.

So no matter what decrease there might be in their A1c after adding Lantus to their daily regimen, the person with Type 2 who takes Lantus and continues to eat a high carbohydrate diet is heading for a very ugly future.

The only insulins that can lower post-meal blood sugars are the fast acting insulins, Regular Human Insulin (Humulin or Novalin R), Humalog, Novolog, and Apidra. Those insulins must be dosed very carefully to match the amount of carbohydrate in each meal or they won't be effective either.

Unfortunately, it takes time to educate patients about how to match insulin to food. Time doctors don't want to spend on patients because it is very poorly reimbursed by insurers. So most people with Type 2 Diabetes do not have access to the well-trained diabetes educators who could teach them how to use fast acting insulin and match it with their food. Instead doctors turn them over to the care of a nurse who may have learned all she knows about insulin 20 years ago and whose main concern when she faces a patient is to avoid hypos by keeping the doses of insulin that patient uses low enough that the patient rarely sees a blood sugar lower than 180 mg/dl.

The sad truth about insulin is that it takes intelligence and study to use it correctly and most doctors don't credit their patients which having either the ability or motivation to learn how to use this powerful, life-changing drug correctly.

If you are willing to put in the time to learn to use insulin correctly, you can get very good control. Read these books: Dr. Bernstein's Diabetes Solution by Dr. Richard K. Bernstein, John Walsh's Using Insulin, and Gary Scheiner's Think Like a Pancreas. Each of these books takes a different approach to both diet and dosing, but reading them all should give you some insight into how to approach using insulin so that you can tailor your own dose to your own diet and exercise level.

After you've read these books and have a better idea of what is involved in using fast acting insulin, if you think you need fast acting insulin, keep at your doctor until he prescribes it for you or refers you to an endocrinologist who will.

If your doctor does not send you to a competent diabetes educator, or if after reading these books, and doing what the diabetes nurse suggests you are still seeing dangerously high blood sugars, visit one of the support communities you'll find online like Tudiabetes.com, diabetesdaily.com or diabetesforums.com and discuss your situation with the people there who use insulin to get excellent control.

Even though you are a Type 2, you may find that Type 1s have a lot to teach you because they generally get much better diabetes education than do any Type 2s. If you listen carefully to people using insulin whose control is excellent, read the suggested books and pay attention to what their authors are trying to tell you, and cut back on your carbs as much as possible, you should be able to get your blood sugars back into control. Many of us have done it.

Scare of the Day: Diabetes & Alzheimer's

2008-04-10T16:03:00.011-04:00

Yesterday's bit of depressing news for people with diabetes is a Swedish study that is being reported in the news with headlines like "Alzheimers Risk Tied to Diabetes in Middle Age"

The abstract of the actual study is HERE
It is titled, "Impaired insulin secretion increases the risk of Alzheimer disease."

Apparently they gave a group of 2,322 men intravenous glucose tolerance tests in 1970 and then followed them for the rest of their lives tracking which ones developed Alzheimer's disease and dementias.

The researchers conclude, "A low insulin response at baseline was associated with a higher cumulative risk of AD. Impaired glucose tolerance was associated with a higher risk of vascular dementia."

Unfortunately, from the brief description available in the free abstract, it isn't clear what they actually measured. They did intravenous glucose tolerance tests, but the way the report mixes the terms "insulin response" and "insulin resistance" does not make it clear whether they are talking about low insulin secretion or high insulin resistance, and these are two very different metabolic issues.

[NOTE: Dr. John Griffa informed me that the study DID measure insulin levels.]

Beyond that, though, before we conclude that it is only time until our brains are toast, we have the problem, once again, that the study is not able to tell us whether the brain damage was caused by the underlying condition that causes insulin resistance and/or insulin deficiency of if it was the result of long term exposure to the high blood sugars that doctors fail to treat aggressively in people who have either insulin resistance or insulin deficiency.

If it's something in the genes causing the damage, well, a lot of us are screwed. But if, like so many other diabetic complications, the damage is done by exposure to high levels of circulating glucose which gradually clog up the works all over the body, we aren't.

And in a world where doctors tell patients that A1cs of 7.2% are "great control" and refuse to give any treatment to most people with Type 2 diabetes until their A1cs are well over 8%, most people with IR and insulin deficiency under a doctor's care are walking around with very high blood sugars indeed. So we aren't likely to see any studies that look at the incidence of either Alzheimer's or dementia in people who keep their blood sugars in the normal range, no matter what their IR or insulin secretory capacity.

If this latest report worried you, remind yourself of this: No matter how bad your blood sugar might be, it is possible to get it back to normal levels. The tools are simple and well known.

1. Cut way back on carbohydrates. It is carbohydrates that raise blood sugar and the less carb you eat the less of a rise you will see in your blood sugar.

2. Exercise if you can. Exercise reduces insulin resistance and encourages glucose uptake in muscle cells.

3. If diet and exercise don't do the job, investigate which of the available, safe diabetes drugs might work for you.

4. If oral drugs don't work, use insulin and insist that your doctor work with you to find a dose that gives you good control.

Far too many doctors do not know that people with diabetes can get normal blood sugars. Hence their belief that the 7% A1c that represents an average blood sugar near 170 mg/dl is "good control." Even more doctors dismiss the blood sugar levels defined as impaired glucose tolerance as merely, "Nothing to worry about." This study makes it clear that they are more than that. Unless you think being demented is nothing to worry about.

A lot of recent research makes it pretty clear that blood sugars are over 140 mg/dl 2 hours after a meal very slowly damage capillaries, nerves and retinas. Now this new study suggests they are also clogging up the tiny veins in the brain.

But until there is some definitive proof that it is the underlying condition leading to insulin resistance or deficiency rather than exposure to high blood sugars caused by IR and ID, that does the damage, there is hope.

And there is also one more reason to strive for normal blood sugars, not the much-too-high blood sugars that the ADA defines as "tight control."

Exubera Linked to Lung Cancer -- Is Januvia Next?

2008-04-09T19:28:00.004-04:00

Today's business news included a story about how Pfizer has found a significantly higher incidence (not risk, actual incidence) of lung cancer in people taking its inhaled insulin Exubera.

Pfizer is no longer marketing Exubera in the U.S., but it continues to sell it to patients who had been on it and test it in clinical trials.

Inhaled Insulin is Cancer for Mannkind - Forbes

What is most disturbing about this story is not just that this cancer finding emerged after years during which Pfizer assured the medical community that Exubera was completely safe for the lungs. That's nasty enough. But what is most disturbing, to me, is how this finding highlights how inadequate the current system of clinical trials is for determining if a drug that uses a novel mode of action promotes cancer.

Yes, the clinical trials will determine if exposure to the drug causes cancer to grow in a test tube and it will also test to see if 60 times the human dose of the drug causes cancers in rodents. But whether a normal dose of the drug changes the balance of the human body in a way that might allow cancer to grow where it otherwise would not grow is NOT investigated. Nor do most clinical trials run long enough for slow growing human cancers to become evident. It is only after a drug is used by tens of thousands of paying customers that its ability to cause cancers usually emerges, as was the case here with Exubera.

Few patients ever used Exubera. But I have been writing for more than a year now about why the most frequently prescribed new diabetes drug, Januvia, poses a very real cancer risk that has not been investigated at all. The way Januvia promotes cancer makes it very tough to connect those cancers to the drug, since the cancers it may promote is melanoma.

When someone is squirting a drug into their lungs and develops a lung cancer, the doctor may make the connection between the drug and the cancer. When someone is taking a pill to lower their blood sugar and dies of melanoma, the doctor probably won't. They'll think, "Too much sun." Not, "Januvia turned off the enzyme the body relies on to kill melanocytes that have gone malignant."

Doctors do not understand that Januvia inhibits the action of a protease, DDP-4, that appears to play a part in the immune system's fight against cancer. Doctors know only that that inhibiting DPP-4 raises GLP-1. I suspect if you ask your doctor what DPP-4 is, you will not get a coherent answer, because busy doctors have very little understanding of the biochemistry of most of the drugs they prescribe. And even if your doctor does know what DPP-4 is, he isn't likely to know that DPP-4 is used in the immune system and that it is active in the brain. Mine didn't.

And when a pretty drug company rep chirps, "DPP-4 inhibitors lower glucose" you doctor certainly didn't ask, "When you inhibit this molecule with your drug, what else are you inhibiting?" Even worse, when approving the drug, the FDA didn't ask that question either. There was NO study submitted as part of the drug approval process for Januvia that investigated the impact of inhibiting DPP-4 on its specialized functions throughout the immune system.

We do know that another drug, Ankinra, which also ends up inhibiting DPP-4, did raise the incidence of melanoma in the population who took the drug for a longer time than the Januvia trials lasted. But because the clinical trials for Januvia did not last longer than two years and the cancers involved take more than two years to develop, if we do get a rash of unnecessary cancer deaths due to this drug, the connection may never be made.

This is very worrisome. Ever since I first published the links to the research conneting DPP-4 inhibition with melanoma I have been waiting for someone to write me, "Foolish woman, there is no reason to worry about this issue because . . . " followed by a long list of cogent reasons involving knowledge of biochemistry and physiology far superior to mine.

But no one has. One researcher told me that I had raised a valid issue but that no research had been done to look into it. And that's all I heard.

In an ironic way, the Exubera report is GOOD news, because the connection was made between the cancer and the drug. With Januvia, that may not happen. So I urge you to report to the FDA Medwatch Program any skin cancer you contract while taking Januvia. If you hear of any such cancer occurring in a person taking Januvia, insist that they get their doctor to report it to the FDA. This may be the only way we save hundreds or even thousands of lives from a very nasty and very unnecessary death.

Lab time again

2008-04-07T13:42:00.007-04:00

I get labs every six months. This time my doctor checked my B-12 and Vitamin D levels, along with the usual stuff.

My A1c was 5.7%. That's pretty much what it always is. I had a cold last week and my blood sugars were higher than usual, so actually this A1c is better than I expected. It was 5.8% last October.

Using the most recent formula to equate A1c with blood sugar level, the one described HERE. this equates to an average blood sugar of 117 mg/dl.

My many meter readings are always lower than any A1c formula predicts, which suggests that I'm one of those people who is a high glycator. That topic was discussed HERE

My meter shows that my actual blood sugar average is closer to 100 mg/dl. But the biggest problem I have with blood sugar is my fasting blood sugar. I have a ferocious counter-regulatory response that fights all attempts to lower it. If I use even 1/4 of a unit too much Lantus, I'll wake up at 4AM with heart pounding and blood sugar at 107 mg/dl--a sure sign that I dipped into the 70s and caused that counter-regulatory response. If I don't use any insulin, even with a very low carb diet my fasting blood sugar will be in the 120s. So for now, I do what I can during the day to keep the blood sugar down. I'm still trying to tweak the Lantus dose to find one that will work, but for now my morning fasting blood sugar is 98-108 though I can get it to drop into the 80s during the day.

At my endo's suggestion, I've been supplementing with 1000 IU of Vitamin D every day for six months. My Vitamin D level was 39.8, with the normal range range being defined as 32-100 ng/ml. So it looks like I can boost my Vitamin D level without worrying about overdosing.

I'm using Vitamin D for its supposed usefulness in fighting melanoma not for any supposed effect on blood sugar. Though I initially saw a strong impact on my insulin sensitivity when I started the Vitamin D supplementation--I was hypoing on normal doses of insulin--it wore off very quickly. Now Vitamin D has no effect at all on my insulin sensitivity. Vitamin D does seem to improve my mood through the dark, short, sunless days of a New England winter. Plus, anything I can do to discourage rogue melanoma cells from taking root is all to the good.

My Vitamin B12 was on the high side, so that's good. Metformin can deplete Vitamin B12, so it is a good idea to check it every year if you are taking metformin.

My cholesterol was excellent. As usual the total was very high--I have that "longevity" variant of cholesterol that Dr. Nir Barzilai identified in the Albert Einstein Medical School Longevity Study. This gene makes for very large, "fluffy" LDL and HDL particles which tend not to clog arteries. My dad's cholesterol was measured at 340 when he was 70. I got into that study because he was a centenarian.

For the complete list of Longevity Study publications, click HERE.

So when I look at my cholesterol test result, what I look at is triglycerides and HDL. When I'm eating the right amount of carbohydrate and have my insulin set right, TGs are low and HDL is high. This time my HDL was 76, which is the highest it has ever been, and my TGs were 83 which is very healthy.

So I'm happy. But my doctors will probably look only at the total Cholesterol number which is 294 and have fits. That is what they always do. I have printed out data about the study and explained to them that I was informed that I do carry the longevity variant of CETP, and I have asked them to put it in my file, but it makes no difference, since none of them ever read my file but only look at the latest lab sheet.

My microalbumin test was great <3.0 with normal being defined as 0-20 mg/dl. The ratio of microalbumin to creatinine was <3.2, which is also great.

So basically, if I don't walk into the path of an oncoming car, or contract MRSA, or get bit by the wrong mosquito this summer, it looks like I should be around for many years to come.

Lastest News about Blood Sugar 101, The Book

2008-04-05T10:16:00.007-04:00

For those of you who ordered my book directly from Technion Books using the Pre-Publication Offer, it has been taking about 10 days for the Post Office to deliver books that are shipping to the Midwest or West Coast.

The very first books ordered, which shipped to California on March 26 arrived there yesterday. So be patient. Your books are on the way!

There have been some really nice reviews cropping up on the web. The best was at dLife Blogabetes.

There's an fine reader review at Amazon, too. If you like the book, I would encourage you to post reviews on both Amazon and Barnes & Noble online so that people who aren't familiar with the blog and web site have a chance to learn about the book.

The pre-publication offer is over. Technion Books now offers U.S. customers the option of ordering via Priority Mail, which should arrive in 2-3 days, or by the less expensive but slower Media Mail. Books will be put into the mail within 24 hours. Order in the morning and your book will go out that afternoon.

Order from the publisher at Technion Books.

You can also order Blood Sugar 101 from Amazon and Barnes & Noble Online.

The Email I Have Not Received

2008-04-04T10:45:00.007-04:00

I get a lot of emails in response to the postings on my Blood Sugar 101 Web site. People write me with comments, questions, and requests of all kinds.

I file each email away into the appropriate folder. I was as I was doing this today, it occurred to me that there is only one kind of email I do not see, and that is one that says, "I followed the advice I saw on your web site, lowered my blood sugar, cut back on my carbohydrate intake, and it made my health worse."

Given the contentiousness of the web, I would expect to see such emails. After all, the ease with which anyone can set up a completely anonymous email account makes it very easy to send such an email. We all known that anonymity encourages people to indulge in behaviors they would never consider if they knew that their identity could be tracked down. So you'd think that in the normal course of events I would get a couple of emails of that type.

But I don't. Instead, I get emails from all over the world from people who tell me how surprised they were at the ease with which they could recover their blood sugar control once they understood that carbs are what raise blood sugar and that cutting back on carbs is the best way to lower blood sugar. I also hear from people who tell me that my web site gave them the courage to go in to their doctor and demand insulin after cutting carbs could not get their A1c below 7%, who tell me how hard it was to convince their doctors that the ADA's recommended blood sugar target was too high to provide them with health and safety.

I also get emails from people who tell me how lowering their blood sugar improved the pain in their feet and how they wish their doctors had told them that, rather than putting them on expensive medications which had unpleasant side effects.

I mention this not in defense of my advice--it needs no defending, but because it highlights how heinous it is that now, a decade since advice like mine first made it into the mainstream, The American Diabetes Association continues to whine that the strategies I promote "Need further study" and still refuses to put the word "carbohydrate" on its "tight control" web page.

The ADA does this despite a decade worth of research that has proven that for people with diabetes the low carbohydrate diet lowers blood sugar and lipids and improves health far more effectively than the expensive oral drugs that may be their alternatives. And the ADA still tells doctors that the 7% A1c is all that is required for people with Type 2, which in effect means most family doctors do not start drug treatments of any type until their patients have had an A1c over 8% for at least a year.

The ADA continues to behave as if cutting back on carbohydrates and shooting for a normal blood sugar might have some hitherto unrevealed negative consequences so dire that they cannot recommend either strategy to the doctors that treat millions of people with diabetes.

It does this at the very same time that it advises patients to keep taking drugs like Avandia whose negative impact on health has been so well documented that only people with a hefty investment in the drug companies that manufacture them or who are on those companies payroll could justify advising people to keep taking them.

But of course, the ADA for all practical purposes is on the payroll of these drug companies. The drug companies are major contributors to the ADA and major funders of the enormous salaries earned by the ADA's executives, none of whom, I believe, actually has diabetes, though they do have professional resumes filled with jobs as health industry and drug company lobbyists.

A friend of mine just got back from her doctor with a prescription of Humalog, which she needed badly and an armful of brochures, many with the ADA stamp of approval, urging her to eat a diet rich in bananas, raisins, whole wheat bread and oatmeal--a diet guaranteed to raise blood sugar.

I'd urge you to write to the ADA to share how badly you fared while eating that particular diet, except that long experience has taught me that the ADA does not respond to emails from us folks with diabetes. We aren't their priority.

The only time they think about us is when they hire telemarketers to call us up and ask us for money. Otherwise, our emails go into the dead letter bin. Where all that money they raise goes is unknown. About a million dollars worth of it goes to their top executives. The rest of it seems to go into those brochures urging people to eat the high carbohydrate foods that will worsen the health of people with diabetes.

If there is one thing that really "needs further study" it is this: How did an organization funded almost entirely by companies who profit only when people with diabetes have poor control and staffed by people who do not have diabetes become the major authority informing doctors how to diagnose diabetes and treat diabetes?

How is it that people who have never tested their own blood sugar after a meal once in their entire lives and who have close ties to those who earn the most money when your blood sugar goes south get to recommend diets to those of us who do?

And most importantly, what will it take for people with diabetes to make their voices heard by the ADA's top leadership, who currently give far more access to drug company executives and junk food industry lobbyists than they do to any of us who actually have diabetes.

If you can figure that out, send me an email. I'd really like to know!

P.S. Full disclosure: I was thrown out of the ADA's bulletin board by the ADA's appointed moderator who accused me of trying to promote my "agenda." As long as my email box fills with letters from people who tell me that my "agenda" changed their lives and health for the better and that they wish their doctor listened to people like me instead of the ADA, I will continue to do just that!

Compared to What? What's Wrong with the Latest Actos Study

2008-04-01T07:57:00.007-04:00

The medical media yesterday were touting Dr. Nissen's report to the big cardiology conference about his latest study of Actos. Here's the headline that accompanied the report in Endocrinology Today:

Pioglitazone may slow progression of atherosclerosis in patients with type 2 diabetes.

But take a look at the actual JAMA journal article this presentation was based on. Its title is: Comparison of Pioglitazone vs Glimepiride on Progression of Coronary Atherosclerosis in Patients With Type 2 Diabetes: The PERISCOPE Randomized Controlled Trial.

What should immediately leap out to you is that in this study Actos' effect hardened arteries was being compared with Amaryl, a sulfonylurea drug which is part of a drug family that has long been suspected of worsening heart disease. Not a placebo.

This was a small study. Only 543 patients participated, split into two groups, but 90-some patients in each group dropped out. This left only about 180 subjects in each arm of the study. To their credit, the researches cite the small study size and the unusually high drop out rate as a possible problem.

The study only enrolled people who already had evidence of blocked arteries. It concludes that, compared to those taking Amaryl, patients taking Actos saw a tiny though statistically significant decrease in the thickness of problem arteries. They had improved CRP (a measure of inflammation) and HDL though there was no actual difference between the number who died in both groups during the study.

The group taking Actos had slightly better fasting blood sugars and fasting insulin levels than those taking Amaryl, though of course, as is the case in every drug study you will ever see, their actual fasting blood sugars were high enough to damage all their organs.

A cheery graph shows the average fasting blood glucose of each group. The group average of those taking Actos started at 147 mg/dl and dropped by 8.5 mg/dl by the end of the study.

But this graph ignores the standard deviation of the group. The standard deviation is a measurement of the range within which most of the values in the group cluster. In this study, the standard deviation for fasting glucose was 41. That means that most of the fasting glucose values clustered between 106 mg/dl and 188 mg/dl.

But here's another concern: though standard deviations are presented for the starting values and measurements in the middle of the study, no standard deviation is given for the amount of improvement experienced at the end of they study. That is presented as an average with a confidence interval--the latter being an estimate of how accurate that average might be. This is far less informative than information about the standard deviations of the individuals' improvements might have been. So it is possible that the inclusion in the group of several people who were very strong responders to the drug could have skewed the final result.

Averages presented without their standard deviations should always be treated with great caution. If you average my income, your income, and that of Bill Gates the amount you come up with could be $500,000,000. That's because you get an average by adding all your values and dividing by the number of values. But standard deviation would show you how misleading that average is, because it might be $499,950,000 telling you that values averaged fell in a range plus or minus $499,950,000. This example should show you why averages are meaningless without knowing the standard deviation.

A far better measurement of values in a group is the median, a measurement which lines up all your values in order of size and picks the middle value. The median of your income, my income, and Bill Gates' income is likely to be something like $50,000--a more informative statistic.

More importantly, by pooling group data and using averages to analyze the group, we miss the really important statistic: the actual change per individual. Though the authors present a dizzying description of highly confusing statistical techniques they used, ones I doubt anyone but they themselves could understand, one wonders why they did not simply look at the increase and decrease per individual of the parameters measured and present the median and standard deviations of these individual changes which would have been far more informative.

That said, Dr. Nissen has a very good reputation in the field, so lets give him the benefit of the doubt and conclude, as he did, that Actos did make a very small improvement in the thickness of arteries in the people who took Actos compared to those who took Amaryl.

It is time to ask your doctor for some Amaryl?

Probably not. There were two other statistics buried in this study that should give you pause. Both of them relate to the most troubling side effects of Actos.

We all know that one of the biggest problems with the sulfonylurea drugs is the weight gain they cause. Well, this study showed that people taking Actos gained more than twice as much weight as those taking the sulfonylurea drug, Amaryl. Not only that, the standard deviation of the weight gain in the middle of the study was much larger for those taking Actos, suggesting that some people on Actos gained a lot more weight than the average would suggest.

We know that Actos lowers the insulin resistance by growing baby fat cells and stuffing them full of new fat. These cells, once grown, will never go away, which is why people who gain weight on this drug report that even after they stop taking it, getting rid of the additional weight is extremely hard if not impossible.

The second side effect is worse: There were no bone fractures in the Amaryl group, but fully 3% of the Actos group experienced bone fractures.

It is now well known to those of us who learn about drugs from sources other than manufacturer-funded studies that Actos builds those baby fat cells we mentioned above by hijacking the stem cells that should have turned into new bone. Over time this leads to osteoporosis, and there is no doubt that Actos causes osteoporosis in older women, a group whose thinner bones are more likely to fracture if weakened.

This study lasted only 18 months but there was still a very significant difference in the number of fractures between the two groups. So the high number of fractures--8 in this group of less than 200 people of mixed gender and ages taking Actos is extremely troubling.

Actos is a drug people will be put on not for months, but for years or even decades. Osteoporosis is one of the major killers of older women who break hips and then almost always die. So how Dr. Nissen can dismiss this drug as having a "reasonable safety profile" is beyond me.

And finally, whatever this drug did to artery thickness, there was no significant difference in actual mortality outcome in this study and, indeed, there were more fatal heart attacks in the group taking Actos. This study was short, but the other worrisome side effect of Actos in people who take it for longer time periods is that it produces congestive heart failure in people who did not have it when they started taking the drug. This is probably due to the edema (water swelling) it causes. It will be cold comfort indeed to know that your arteries are some tiny fraction thinner when you discover you have stretched your heart muscle to where it can barely function and that thanks to heart failure, your chances of surviving eight years is one in five--far worse than those for people with cancer.

More Insight into Who Should Take Statins

2008-03-31T12:04:00.006-04:00

You will be seeing a lot of news coverage coming out of this week's cardiology conference about a large study of the statin drug, Crestor, which supposedly found it cut cardiovascular deaths in a group of people with normal LDL better than a placebo.

What most news coverage is leaving out is this: The group of people with "normal" cholesterol who took Crestor in this study weren't just any old group of people. They were people with elevated CRP.

This is an important distinction. CRP stands for C-reactive protein and it is a measure of inflammation. Earlier studies had shown that statins are only helpful in reducing cardiovascular events in people with pre-existing heart disease. Accumulating evidence suggests that they do this by reducing the artery inflammation that is characteristic of heart disease, not by reducing cholesterol. There has never been any truly solid proof that high cholesterol in and of itself causes heart attacks.

So this latest Crestor study may actually have done to finally narrow down who it is who should be taking statin drugs to the subgroup of people, whatever their cholesterol might be, whose CRP is elevated.

Given the way this new story is being reported, I'm not sure we can count on the drug company to give doctors thats message. Instead, the message might be that everyone, no matter what their cholesterol might be, should take this expensive drug.

This might be a mistake. Statins cause serious and sometimes irreversible side effects, some of them affecting mental function. They are particularly dangerous in older people.

If your doctor wants you to take a statin, demand that you first have a CRP test. If your CRP is normal and you have not been diagnosed with heart disease using a definitive diagnosis from something like an artery scan, rather than an inference from something like a high cholesterol test value, you may not need the statin.

I've done this myself, and my CRP was rock solid normal. That is one reason I have been very resistant to the idea of taking statins no matter how high my LDL might be. I saw a statin cause almost instant deterioration in my dad's hitherto stellar mental functioning, and no way am I gambling with mine!

Another piece of Crestor news is that a smaller study, which reanalyzed results of the Asteroid trial, found evidence of some regression in artery plaque in people taking Crestor. This particular trial did not investigate whether the changes observed actually mapped down to fewer heart attacks.

Also, keep in mind that these are reports at a convention, not peer reviewed research studies, and we won't really know how significant the findings were until we see the actual data in a publication. We also won't learn about the side effect profile of Crestor that was observed in these trials.

So, as is usually the case, the devil may well be in the details. For now, it's worth noting that most of the coverage of these reports is in the business press because the bottom line is that $tatin$ are all about profit$.

Here's one of the more informative reports about these studies:

Another Blow for Schering and Merck