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

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

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?

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

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!

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

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

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.