October 29, 2007

What Taubes Has Proven and What Remains to be Studied

Thinking over the Taubes book, Good Calories, Bad Calories, I've been struck by two things: What he has proven and what it is that he didn't discuss that is just as important as what he did.

What Taubes Proved

1. Taubes proves beyond a shadow of a doubt that the quality of nutritional research published in mainstream journals over the last 50 years is abysmal

2. Taubes proves beyond a shadow of a doubt that the Cult of Personality allowed politically powerful experts to impose their theories on the health community even when the research did not support their theories.

3. Taubes proves that the belief that eating saturated fat causes heart disease has never been well supported by the data and that cutting back on eating fat and replacing fats with carbohydrates has never been shown to reduce the incidence of heart disease.

4. Taubes proves very solidly that the belief that a low fat/high carb diet prevents cancer has never been supported by any well-conducted research and that, in fact, it is possible that lowering cholesterol may promote rather than prevent some cancers.

5. Taubes proves that most of what "everyone knows" about the causes and treatment of obesity is urban legend and that the findings of the better obesity researchers have been ignored because they do not support the dream that self-control and exercise are all it takes to solve a serious weight problem. In this he pretty much agrees with Gina Kolata's conclusions in her review of obesity research, Rethinking Thin and with what is documented in the even better review of Obesity Research, Fat: Fighting the Obesity Epidemic, by Robert Pool.

The better research seems to show that losing weight once it has packed on is extremely difficult verging on impossible and that Taubes is very right that we need to understand what disorders the metabolic controls that prevent weight gain, because once they are shot, very little helps.

6. Taubes points to some good research suggesting that the huge increase in fructose intake from sugar (sucrose) and high fructose corn syrup may contribute to weight gain and heart disease. Unfortunately, there isn't enough rock solid research to conclude this categorically.

7. Taubes points to some good research suggesting that high triglycerides caused by eating too much fructose may disturb the systems used to regulate metabolism and lead to the accumulation of unnecessary fat.

8. Bottom line: There is a great deal we just don't know about the relationship of diet and health and the best way to deal with obesity. That is because so much of the research done over the past 50 years is of very bad quality, and that this research then gets recycled in "meta studies" that are treated as if they could somehow surmount the serious flaws in data in the studies used to create the meta studies.

Real Progress Could Come From Admitting How Much We Don't Know

Taubes anoints a low carb diet as the solution, but those of us who have been deeply involved with low carb diets for many years and who have gone past the religious conversion stage of low carb dieting know that low carb diets do not solve most people's weight problems and that there are significant problems that keep people from sticking to them long term.

To blame long term low carb dieters for their failure to stick to the diet, blaming either weakness of will or the very suspect concept of "carb addiction" is to fall prey to the same blindered "I know it's true so I'll ignore anything that suggests there are problems" attitude that let the failed low fat diet rule for so long, even though it rarely worked.

My own experience over almost a decade of involvement with the online diet and health community is that Low Carb advocates are just as religious about their beliefs as are the low fat people. They, too, ignore data that does not fit the conclusions they'd like to believe are true.

Low carb diet advocates get angry and abusive if real issues are raised, for example, the slowing of the metabolism on a on long term low carb diet. I've been shunned in more than one online community for raising this issue, and the related issue of possible thyroid problems which is the main problem that got me to stop my very low carb diet after sticking to it for 3 years the first time and 2 the second time.

My take on it for now is that Low carb dieting is more effective than low fat dieting for many people with blood sugar abnormalities, but it does NOT solve all their problems, and maintaining weight loss over time can become very tough as is the case on ANY diet.

Eliminating sugar, fructose, and corn syrup, did not solve my weight problems years ago though I did it for 3 years. It is not a magic bullet. In fact, if 75 years of diet research has done anything, it should have been to teach us there are no magic bullets.

What Was Left Out May Be As Important As What Was Put In Taubes' Book

Some issues that Taubes did NOT discuss that haven't been researched enough and probably won't be, which have a huge impact on health and obesity are these:

1. The impact of the skyrocketing use of plastics to wrap and contain food over the past 25 years on obesity. We know that phthylates seem to have a negative impact on health, but very little research has been done on this huge issue which is one of the biggest changes that has occurred during the period in which obesity rates have leapt.

2. The impact of various chemical additives used in packaged foods and fast foods on obesity, cardiac health and cancer. The list of preservatives and mysterious sounding additives like "dough conditioner", "texturized protein,", "hydrolyzed plant protein", as well as the many other chemicals used in prepared foods and restaurant foods is much longer than it was 50 years ago.

Few of us know much about these chemicals. Even worse, we do not know anything about the chemicals that don't appear on the label but may be in our food since so many food additives are imported from China where they are polluted both intentionally and accidentally, especially with the industrial chemicals and pesticides in Chinese water.

3. The impact of pesticide residues in our foods on our health and the mechanisms our body uses to maintain weight homeostasis. Our foods are full of pesticide residues and there is for all practical purposes NO EPA oversight in this area anymore.

4. The impact of industrial chemicals which are found in our air and water and get into our foods as they grow.

5. The impact of hormones and hormone mimics in water supplies which have become significant enough to cause sexual changes in some fish and amphibians exposed to them.

6. The impact of changes in the amount of exposure to radiation including X-ray and microwave radiation.

7. The impact of adding soy and soy byproducts to almost all prepared foods, even things like bread. The dangers of soy are well described in The Whole Soy Story by Kaayla T. Daniel. This book is as well researched as Taubes' book and it should be MUST reading for anyone who cares about food and health. Daniel shows the same pattern of fatally flawed research was used to turn an industrial byproduct into a supposed "health food" and documents a long list of serious health problems caused by soy in our food.

If obesity is caused by gluttony and sloth rather than poisoning from plastic soda bottles, soy in our foods, pesticide residues, and industrial chemicals people can feel safe.

But if obesity and metabolic diseases are increasing at a frightening rate because of the emergence in the mid 20th century of plastics, pesticides, and toxic clouds of industrial chemicals which saturate the air and soil, no one is safe--though industry is not going to want to pay the price for making the changes needed to end the "epidemic" and industry has so corrupted our politicians that you won't ever see this issue getting any press. Which is one reason why any theory that blames people who are experiencing metabolic failure on those people's moral failings is going to continue being attractive to the people running industry and government

Meanwhile, the mainstream response to Taubes' book seems to be mostly petty debates about his interpretation of this or that cited study rather than an acknowledgment that his main finding is very true: most of our nutritional and health research has been sloppy crap and WE DON'T KNOW SQUAT ABOUT THE STUFF THAT MATTERS.

October 25, 2007

Taubes Good Calories Bad Calories - A Lost Opportunity?

I recently got a copy of the new Gary Taubes book, Good Calories Bad Calories, which a lot of us have been waiting for with high hopes.

Alas, this was not the book I had hoped it would be. Taubes has done a heroic job of studying and analyzing the history of 75 years worth of dietary research. No one with a shred of intellect can read this book without coming away convinced that the Politics of Personality caused nutritional research to go where the data never led it and to spend 40 years wandering in that high carb/low fat desert.

But the Taubes book is 600 pages of some of the densest writing I've encountered in a long life of reading popular science. How dense? Well, I managed to sprain a finger reading it, that was how heavy it was. And the prose is just as dense as the paper. Long convoluted sentences that just don't come up for air, and explanations of technical issues so impenetrable that they left me scratching my head trying to figure out what the heck was he talking about.

And I'm someone who reads a lot of big fat information dense books. For example, I just this week read, and loved Vaccine: The Controversial Story of Medicine's Greatest Lifesaver by Arthur Allen which covered as much controversial medical research history as Taubes does and was a similar length.

But where I was reading the Allen book with the kind of excitement with which I read a good detective story, because Allen made his line of argument very clear no matter how much data he introduced, with the Taubes book every fifty pages or so I found myself taking deep gulping breaths and skimming despite myself because Taubes had just plain buried me under the weight of his data.

And if I had that reaction--a person who reads at least a dozen health and nutrition research reports every week and often more--I cannot imagine what Joe Public would make of this book. Indeed, as someone who led a long and happy career in nonfiction publishing I am bewildered as to who exactly it was written for. To me it seemed as if the target reader was envisioned to be someone who reads Science at the breakfast table and then digs into Nature on the train to work. If there are enough of those folks to make this book a success, I'm all for it.

But my impression just looking at the title, cover and packaging is that Good Calories Bad Calories is being marketed to the diet book buyer. Who is going to get about 25 pages into this book and then fall dead from exhaustion.

That is probably why it is looking like this book is only getting discussed online by the hard core diet wonks who already know what it is that Taubes is trying to document: that the mainstream dietary advice that blames saturated fat for heart disease and recommends a high carb/low fat diet as "healthy" was never based on good scientific research and that carbs in general and fructose in particular are probably what is causing the so called "obesity epidemic."

But if the only people reading the book are those who already know what it has to teach us, it's a failure. Which is tragic. Because its core message is VERY important. Fat has never been proven to do any of the things "everyone knows" it does and high carb/high sugar diets are just plain killing people.

If I had a buck for everyone who told me they are eating a low fat diet to lower their cholesterol and prevent heart disease I'd be rich. Ditto all the doctors convinced that saturated fat is what causes heart disease. Reading this book could cure that. But I can't see those people reading this book.

So I came away wishing that there was some way that Taubes could come up with "Taubes Lite"--a 250 page book that would extract the "pearls for practice" buried in his data and pitch that book to the person trying to figure out what a "healthy diet" might be. Something that would help people with diabetes understand why the ADA insistence that they should eat all the sugar they want is dangerous, and get the media to understand that obesity is not caused by overeating. It is caused by eating foods that short circuit the metabolic systems our body uses to keep our weight in homeostasis, foods high in carbs and fructose.

But it ain't going to happen with this book, and that's a damn shame.

October 23, 2007

More Bad Science: Cereal for Breakfast

Your friends in the grain business have been busy promoting the latest study that supposedly shows that eating "whole grain breakfast cereal" prevents heart failure.

Whole Grains Do a Heart Good

As reported in U.S. News and World Report: "Compared to those who ate no whole-grain cereal, men who consumed 2 to 6 servings per week saw their risk of heart failure fall by 21 percent, while those who ate 7 or more servings per week reaped a 29 percent reduction in risk, the researchers reported in the Oct. 22 issue of the Archives of Internal Medicine."

What's wrong with this study?

Well, for starters, we know nothing else about the weight, diets, ethnic heritage, and lifestyle of these people who ate whole grain cereal for breakfast, but it is very likely that they ate those breakfasts because they have been touted as "healthy" and that eating the cereal rather than causing the outcome was a marker for a lifestyle high in exercise, weight control, ethnic background, and other behaviors likely to impact health.

Using the same logic, you might be able to prove that people who owned a specific brand of running shoe had a lower "risk" of heart failure. Did owning the running shoe cause the health outcome? No. If you buy that running shoe and wear it while watching TV you won't improve your health.

The other big problem here, as usual is that you are comparing people eating one high carb breakfast with others eating an even higher carb breakfast. So yes, I'm willing to believe that eating granola for breakfast might be healthier than eating Sugar Frosted Flakes, but I'd really like to see what happens when you compare people eating the grain breakfasts with those eating NO carbs at breakfast.

Most importantly, the study did not separate out people with Diabetes from those with normal glucose tolerance. We know for a fact that anyone with Type 2 diabetes who eats a grain cereal for breakfast is likely to see their highest blood sugar of the day after breakfast, because of the natural increase in insulin resistance we all experience in the morning. And we also know that cumulative exposure to high blood sugar leads to bad health outcomes. In addition, people with diabetes are more likely to experience heart attacks--not being measured here--rather than heart failure, which usually develops in people who survive heart attacks.

This raises an important point: The condition being studied was "heart failure"--a condition in which people suffer weakened heart muscles--rather than heart attack, and that the measurement being used was "risk of" which is very different from "incidence of".

The Risk statistic is used to amplify very slight differences between the incidence of a condition in large groups of people, and is almost always used to make a very small effect look more significant. If you reduce the number of people in a group of 100,000 who get a heart attack from 10 to 8 you've made a huge difference in risk but a very small difference in incidence. But if you are trying to promote a drug or product, citing risk rather than incidence makes your product look like it makes a huge difference when it doesn't.

These studies seem to be more of the same kind of "let's prove what we believe to be true by ignoring rigorous analysis of the data" research that Gary Taubes highlights so brilliantly in his book, Good Calories, Bad Calories.

By the way, the nutritionists in the article recommend that you eat your high carb whole grain cereal with high carb low fat skim milk and fruit. More proof, if you needed it, that religious beliefs can not be challenged by logically supported argument. Sadly, no matter how densely documented the truth might be (and Taubes documents it to the point where it exhausts even ME, which makes me wonder exactly who his target reader must be!) the belief in the value of the high carb/low fat diet will not go away no matter how much more rigorous research shows it to be a flop.

Meanwhile, if you have diabetes and are tempted to breakfast on granola with skim milk and bananas, by all means do so. Just be sure to measure your blood sugar at 1 hour and 2 hours after eating. If you can get normal blood sugar values at those times (under 140 at 1 hour, under 120 at 2 at a bare minimum--under 100 at 2 hours is better) keep eating like that. If you can't, consider switching to a low carb breakfast of ground flax, protein powder pancakes, eggs, or meat.

October 22, 2007

Vitamin D lowers Insulin Resistance?


Research published after this blog post was written finds that supplementing with Vitamin D, even in intravenous megadoses does NOT improve blood sugar or insulin resistance in any significant way. You can find citations to that research HERE.

Vitamin D may have some positive effects on heath, and I continue to take it, but it will not reverse any already existing autoimmune condition nor is it a diabetes cure. In fact, my own blood sugar stopped responding to Vitamin D within a week after I wrote this blog post.

If you found this page searching for help with lowering blood sugars, please check out this page: How To Get Your Blood Sugar Under Control. I hear every week from people who have used this technique to lower their blood sugars dramatically.

Original Post

At my recent visit to the endocrinologist, the doctor suggested I add 1000 I.U. of Vitamin D to my daily regimen because of some recent data suggesting that it helps the body eliminate cells that have developed melanoma.

I followed her advice and started taking a pill every day around 10:30 when I take my metformin. A few days later I started to experience dramatic lows around 3 PM. Lows have rarely been a problem for me, as my body usually mounts an aggressive counterregulatory response at the first hint my blood sugar is dropping. All of a sudden I was seeing blood sugars in the 60s, and they were not resolving with the usual 2-4 grams of glucose. At one point as I battled a low I ended up eating 25 grams of Halloween candy and still only found myself in the 80s ninety minutes later.

It took me a few days to connect the lows with the addition of Vitamin D to my daily regimen. When I did, I started to read up on the relationship of Vitamin D to diabetes. It turns out that the relationship is a strong one, not only for people with Type 2,as a recent metastudy discovered--people with Type 2 appear to have low blood levels of Vitamin D and there is some suggestion that the combination of Vitamin D and Calcium may delay the diagnosis of Type 2, but also for people with Type 1. A Finnish study found that children who received Vitamin D supplementation appear to have a lower rate of Type 1 than those who did not.

There is also some data suggesting that Vitamin D may also be protective against Multiple Sclerosis, a disease that has long been known to be more prevalent in northern latitudes, as well as the data connecting it with cancer prevention.

The large dose of Vitamin D I am now taking appears to increase my sensitivity to insulin even though I am already insulin sensitive. It potentiates a dose as low as 1 unit of insulin, making it several times more powerful than usual. When I have skipped my insulin for a couple meals to see what the Vitamin D it might do when I don't use insulin (while eating very low carb meals) I did not experience the dramatic drop, but I did end up very slowly drifting down into the high 70s a few hours after dinner, rather than ending up in the 90s or low 100s as I would have expected to do.

I have read that it takes many months to completely restore Vitamin D levels to normal, so I'm going to keep supplementing and see what happens,though I'm thinking I might look for a lower dose pill and split the dose to see if I can avoid the dramatic drop all at once, as they are quite disturbing and leave me feeling jittery and off center for hours afterwards.

If you have had any interesting experiences with Vitamin D let me hear about them. I don't know if my sensitivity to Vitamin D is another of the things that grow out of my own, oddball form of Genetic diabetes or something that might be common among people with diabetes in general

October 18, 2007

An Idiot with a Computer Proves Right -- Exubera is GONE.

Scott's Web Log just published the news that in an amazing triumph of common sense over marketing dollars, Pfizer is pulling Exubera off the market.

When Exubera launched, I was quoted in Business Week (complete with horrible photo) as a "typical patient." I said I would not use Exubera because it had some serious problems.

The journalist did not go into what those problems were, though I had spelled them out in some detail, but the main one was that Exubera was a bolus (mealtime) insulin that was supposed to be dosed by the patient's body weight, not by the carbohydrate content of the meal.

That's just plain nuts.

I'm extremely insulin sensitive and dosing Exubera by my body weight would have been likely to send me to the hospital with a severe hypo, as it would have resulted in my taking a dose several times higher than what I actually use. In addition, Exubera was supplied in packs, but a one pack dose was not 1/2 of a 2 pack dose. Titrate that!

Investors did not respond well to my words in Business Week and in the comments section of the Business Week articles I was labeled "an idiot with a computer." I've taken pride in that ever since, and I'm thrilled that the judgment of this idiot with a computer has been vindicated by the medical community who refused to prescribe Exubera despite billions of dollars of money spent on marketing it.

Now if only my warnings on Januvia could get a bit of attention in the media . . . As proud as I am of calling Exubera correctly, this idiot with a computer really doesn't want to be proven right on Januvia by the discovery years from now that it caused hundreds or thousands of unnecessary patient deaths.

BTW, I owe Pfizer this much, that had it not been for the Exubera flap I wouldn't have started this blog. The journalist who interviewed me found me on the diabetes newsgroup, alt.support.diabetes, but described me in print as "a blogger." I figured if I was going to be called a blogger, I better blog, so I did, which has turned out to be a very good decision.

Two Million Human Guinea Pigs

Merck announced recently that patients have filled two million prescriptions for its new diabetes drug Januvia.

Wall Street Journal "Diabetes Drug Wins New Uses

It also announced that new and potentially worrisome side effects have turned up, all relating to the immune system, including rashes and swelling and one potentially fatal condition, Stevens-Johnson syndrome, where the skin literally peels off the body.

Januvia was approved after only 2 years of testing in only a few thousand patients. In addition, as I have pointed out in previous blog entries, the antiquated drug approval system does not require that drug companies look at potential problems caused by novel ways in which a drug functions.

So a drug, like Januvia, that turns off the part of the immune system now known to kill cells that have become cancerous before they become tumors, is NOT tested to see if those kinds of cancers are promoted by the drug. The required drug approval cancer tests only look to see if the drug itself causes cancer in cells in test tubes or in certain animal models which may not develop kinds of cancers humans do.

I cannot say it enough: Januvia changes the way the Immune System works in ways that are not understood by science. It does that by inhibiting the action of an important enzyme/protease, DPP-4, which is used through out the body and brain.

There is no question that Januvia does what Merck claims it does, which is suppress DPP-4, the enzyme responsible for destroying GLP-1, so that GLP-1 levels rise and, in people with living beta cells, stimulate the beta cell to secrete insulin.

But what is not known is what else happens when you suppress an enzyme used in the brain, used to kill rogue cancer cells, particularly melanoma and prostate cancer cells, and for a host of other functions.

Many of these effects may take more than the two years Merck tested Januvia to become evident in the group of patients taking the drug. Because drug companies have every incentive to avoid looking closely at the health of study participants five years after they participate in a drug trial, these long term effects may go unnoticed--or ascribed to chance or other causes, as happened with Avandia.

In addition, because the initial studies were small, severe and even fatal side effects like the promotion of melanoma, might not turn up in these very small study populations. A severe side effect that impacts .01% of a study population and takes 3 years to become evident will not show up on a 2 year study. But with two million people taking the drug, that may translate into 200 people who die needlessly.

A "rare" side effect that shows up in 5% of people taking the drug in 5 years could kill 100,000 people.

Do you really want to take this kind of risk for a small decrease in blood sugar that you could achieve just by cutting out some of the carbohydrates in your diet?

Some people may think I am an extremist, but it's worth noting that I posted on my Main Diabetes Site. about the rashes developing with Januvia almost six months ago. I was the first person to write online about the potential impact of DPP-4 inhibition on the promotion of melanoma.

And just last month, 6 months after I stopped taking Januvia I had another highly suspicious skin growth removed which my doctor told me was well on its way to turning cancerous. He found it unusual for such a growth to appear so suddenly (I get regular skin checks because I am a melanoma survivor.) I did too, which is why I rushed to the skin doctor when I noticed it. It started as a small zit during the period I was taking Januvia.

I only hope that Januvia did not promote the growth of rogue melanoma cells within my body during the three months I foolishly tried it, because if it did, I'll find out only when they are close to killing me. That is how melanoma works, and why you are crazy to be taking a drug, like Januvia, that impacts the system the body uses to kill cancerous melanocytes.

October 17, 2007

Fructose Raises A1c?

Jackie Patti posted an interesting comment to my earlier post about my disappointingly high A1c.

It seems that Gary Taubes' new book discusses this and reveals that fructose causes more glycosylation of proteins than does glucose. However, when we test our blood sugar we don't look for fructose, we only measure glucose, a different sugar.

Hence a diet that is high in fructose may raise A1c, and with it the risk of heart disease and other organ damage, in a person whose blood glucose is very well controlled.

Most people think of fructose as "fruit sugar" as it does occur naturally in fruits and in vegetables like tomatoes and squash which are technically fruit.

But this is only half the story. Sucrose, common table sugar, is 1/2 glucose 1/2 fructose. Honey, which is used in many health foods is higher in fructose than in glucose. And of course high fructose corn syrup is added to most packaged foods including ones you would not expect to have it, things like soup.

It is hard to find nutritional information that distinguishes between the different types of sugars found in other foods, but some helpful web sites list foods to be avoided by people who have a medical condition in which they are not able to metabolize fructose. These sites list wheat as being on the list of foods to avoid, though not rice.

Here's a web site that has the complete breakdown of sugars for many foods, where available. http://www.nutritiondata.com/

So heightened Fructose consumption may explain the rise in my A1c. I have been eating a lot of fresh farm-grown tomatoes and more chocolaty/sugary stuff than is probably good for me, thanks to the extremely good control I've gotten with my insulin. This new information suggests that my higher than desired A1c might be a result of tilting sugar intake too much towards fructose.

If that is the case, much of the problem has already been solved by the turning of the seasons. No more fresh farm stand corn or tomatoes. Back to glucose for treating lows. I'd been using some sinfully yummy hard candies, and that may also have been causing the rise.

I've got the Taubes book on order and can't wait to read the whole thing. Though once I have I probably wont' be able to ever again eat anything I feel like eating without dismay.

October 15, 2007

Food and Environmental Awareness

Since this is "Blog Action Day" I thought I'd talk a bit about food packaging.

It isn't unusual to see someone newly diagnosed with Type 2 diabetes lamenting that they can no longer eat the packaged foods they are used to. But this is a good thing, not a bad thing for many reasons, and one of them is that commercially packaged foods generate huge amounts of waste, especially those packed for "single servings". These "convenience" foods come in elaborate packages made out of plastic wrap, paper boxes, plastic interior packaging, and plastic bubbles, all of which end up in the trash.

When you buy ingredients in bulk and cook your own food, the amount of garbage goes way down. If you are fortunate enough to live where you can compost, it goes down even further, since much of your waste goes out to the pile and become rich garden dirt a few months later.

Kids' lunches are one area where these wasteful convenience foods have really taken over. Juice boxes instead of thermoses, cold cut/cheese/cracker bubble packs, individually wrapped cookies and candies, it goes on and on. None of this is necessary, and the foods you are feeding your kids when you use these kinds of individual servings are very high in carbs, additives, and preservatives many from China. Besides that, there is now some question about whether the plastics themselves may be leaching dangerous chemicals into your child's food.

I get annoyed when I see people making dramatic gestures "for the environment" which have mostly symbolic significance, like turning off lights for one day, while still driving gas guzzler vehicles and generating huge amounts of personal waste.

If you really care about the environment, why not see if you can cut back on the amount of packaging refuse you send to the local dump. Buy ingredients and learn how to cook some of the foods you like to eat. You'll help the environment, and you'll be eating much healthier food while you do it.

October 11, 2007

Got my Gene Test!

The big excitement here is that I finally found a MODY researcher who not only offered me and my daughter a free gene test, but also agreed to share the results of the gene test with us. This is big news indeed.

Not only that, but if I don't have the version of MODY he thinks we have, he said they'd look further into what is going on, genetically. Given that a single MODY gene test can cost $500, and we have gotten conflicting stories from experts about which gene we have, so we'd have to test a few and even then the results might mean nothing, this is like hitting the lottery.

The only other MODY study I found, one being done at Joslin, would have enrolled us in a study if I could have recruited half a dozen relatives, but they were not wiling to share the gene test results, and I don't have that many relatives who would have participated since several of my cousins are adopted.

The gene he is testing is for MODY-2, the form of MODY characterized by a Glucokinase defect. I had previously been told by another researcher that my history sounded suggestive for MODY-1, the HNF4-a MODY, but the second researcher thought that MODY-2 was more likely. Since that is what he is studying, I'm not going to talk him out of it.

The test involves spitting into a little vial, which sounds easy though you'd be surprised how long it takes to get enough spit to fill it. It's going into the mail today and my daughter is sending hers in too. She's the thin, fit, punk fashion model whose blood sugar stays in the 130s for many hours after eating carbohydrates.

I can't wait to find out the result. It would be SO nice to finally have a firm diagnosis, whatever it turns out to be.

BTW, my email box this week has been full of notes from people with family members diagnosed with MODY-2 who seem to have read my earlier blog posting about MODY-2. I have been sending them along to the researcher at his request.

UPDATE: Well, I didn't have the genes they were looking at--probably MODY-2, and the recruiter seemed to lose all interest in me after that. I couldn't find out anything at all about what they'd actually tested for. So that turned out to be disappointing.

For now, I'm not obsessing about it. I've got some kind of insulin sensitive diabetes I've had since I was a 108 pound twenty something (I did get THAT GTT test result). I'm very sensitive to prandin and sulfonylureas. I have a very high renal threshold for glucose which probably rules out MODY-3 So I probably have either the HNF4-a MODY or some other HNF4-a defect which causes the same kind of blood sugar dysfunction. And whatever the diagnosis, I know what I have to do: keep my blood sugar as normal as possible to avoid complications.

More Spinning Statistics to Promote Statins by Drug Cos?

Study: Statin Helps Prevent Heart Attack

Today's health news features a report about a long-term Scottish study that supposedly proves that taking statins for five years lowers the risk of heart attack by 25%. Sounds like everyone on the planet should be taking a statin, right?


Once again, the devil is in the details.

To find out the details, I had to hunt around for reports that gave me the actual numbers involved, since the AP report omits how many people were in the study. Fortunately, a reort in The Scotsman provided critical information left out of the PR release turned AP news story.

Here are the facts:

The study enrolled 6,500 middle aged men [no women] who had extremely high LDL. How high? 192 or over. This is far, far higher than the level at which American doctors tell people they should be taking a statin, high enough that it is clearly abnormal.

Half were put on statins for five years, half on sugar pills. The study stopped in 1995. Over the next ten years 39 percent of the original statin patients were still taking the statins, and 35 percent of the placebo takers were using statins, which of course pollutes the study to the point where it is impossible to draw any conclusions about what happens when you stop the drug.

What was the actual finding?

"Over the 15-year period, 619 of the original statin takers and 674 of the placebo takers died." OF ALL CAUSES.

SO let's do the math. 19% of the ex-statin takers, 40% of whom were still taking the drugs died. 20.7% of the non-statin takers, 35 percent of whom were taking the drugs died. Of all causes.

So in fact, we have a 1.7% difference in total overarall death rate in the two groups. One and a half people per 100. None of the reporting gives the statistics on heart attacks, so it is impossible to know what the real difference in heart attack incidence was in the two groups, but you can be sure that when actual incidence of death is looked at, rather than the factitious "risk of death" measurement which greatly inflates the percentage, it is not going to be high, since obviously many of the deaths were from cancer, accidents, suicide, etc.

More importantly, the study did not look at what the incidence was of dementia in the group of patients taking statins as opposed to those who never took them, a serious concern now that there is some evidence linking dementia with statin use. Nor is there any measurement of "quality of life" issues linked with exhaustion and muscle pain associated with statins.

Finally, it's worth mentioning that without seeing the full data it is hard to know how it might have been massaged to produce the desired result (The study was funded by statin makers and the authors admitted accepting fees from them.) Were the two groups really equal in terms of their cholesterol levels and general overall health?
Often in drug-company funded studies I note that the statistic being used as the prime measurment in a study starts out slightly higher in one group than the other, rather like giving competitors a couple extra feet at the starting gate of a race.

And it is worth noting that this is the only study to date that appears to show that any group of men who had not had heart attacks and took statins had any better survival than those who did not.

My conclusion from this study is this: If you are MALE and your LDL cholesterol is over 192, a statin might be worth taking, but after 5 years, you can probably stop, since the study apparently showed that the very small benefit in terms of life extension--persisted after the drugs were stopped. Though if you are in late middle age, you might want to read up a bit more about the effects of statins on cognitive function before starting them.

Not at all the conclusion that the Press Release turned news report is giving!

October 8, 2007

A1c. Grrr.

I've been seeing the best blood sugars I've had in years these past few months. So I was really curious to find out what my latest A1c would be. My last one was in April and was 5.6%.

The best A1c I'd had since starting insulin was 5.5%, but that was taken two weeks after the Christmas holiday period when I'd been eating what you'd expect me to be eating that time of year, so I figured that was why it was higher than the 5.2% I'd been expecting.

But this time I'd been eating right for months and testing enough that I knew there were no hidden spikes going on. So I was looking forward to a pleasant surprise.

Wrong. The A1c came in at 5.8%.

The DCCT formula suggests that a 5.8% A1c results from running an average blood sugar of 129 mg/dl. No way!

My fasting blood sugar has been a rock solid 92 mg/dl for months. My three hour post meal blood sugars have been in the 90s or 80s. My peaks have been in the 120s, especially the during past two weeks when I'd made some changes to my daily regimen, but even before that I rarely went over 140 mg/dl ever and I was coming down into the 90s after meals.

The highest number I'd seen during this whole time was a single test result of 175 mg/dl which was measured half an hour after eating something starchy when I had injected my Novolog a bit late. Even so, my blood sugar had dropped back to 86 by 2 hours after the meal. And that was almost a month before the test.

The Nathan formula maps that 5.8% to a lower mean glucose number, 107 mg/dl. But that is still 10% higher than any average I see on my meter, total, fasting or post-meal.

Toss into the mix that the A1c is supposed to be heavily influenced by the last two weeks and it gets even sillier. I've been seeing 70s all afternoon the last few weeks.

Another test confirmed that I'm not living in a fantasy by thinking that my blood sugars have improved. My blood lipids were better than ever, in a way that confirmed that my exposure to blood sugars had dropped. With no cholesterol drugs, my triglycerides were 80. My HDL was 76, higher than ever before.

My conclusion is that either a) the A1c is useless for predicting mean glucose normal blood sugar levels or b) I'm a "high glycator" or c) the lab screwed up.

Whatever it is, I'll trust the evidence of my 5-6 blood tests a day over the A1c.

But it is annoying!

October 4, 2007

"Mild" forms of Diabetes that Kill

I recently had an interesting discussion with a researcher who thinks our family history may suggest that we have MODY-2 rather than the HNF4-a MODY which I'd previously been told sounded likely. Even better, this researcher is running a study that will offer gene testing to me and my slim, fit 24 year old daughter whose post meal numbers run in the 130 mg/dl range for many hours after eating.

So that got me looking at the literature on MODY-2 and combing my email files for people who had reported having it. What I found was interesting.

MODY-2 is caused by defects defects--in the GCK gene that plays a significant role in making beta cells secrete insulin in response to rising blood sugars. There are many different defects that cause this form of diabetes, affecting different amino acids in the DNA that makes the gene.

But the diabetes the gene causes is always described in the literature as "mild" and the advice given is that no treatment is needed except, perhaps, carbohydrate restriction. Further reading reveals that "mild" means that this form of diabetes rarely produces the classic microvascular complications of diabetes--retinopathy, neuropathy, etc.

This sounds good, doesn't it!

There's only one problem. People whose families carry this gene tell me that many of their relatives die of heart attacks in their 50s. That's the story in my family, too--two uncles dead before 60 on the side of the family that carries the diabetes gene. One of them was a professional singer and dancer who had been on TV every week only a decade or so before his death, so you can imagine how fit he was. But that didn't keep him from dying of a first heart attack at 58 though he had no earlier warning of heart disease.

If that's "mild" diabetes maybe we better rethink the whole concept of "mild." Dying at 59 with perfect retinas is not exactly my idea of health.

I suspect that the problem here is that MODY-2 is often diagnosed in children and teens, at which time they cause "impaired glucose tolerance" or slightly abnormal fasting blood sugars. So at that time of life, they are mild.

But if they are anything like the diabetes I have, as a person gets older these "mild" forms of diabetes accelerate. In the 40s or 50s, the person may be going well over 200 mg/dl after every meal. Yes, the blood sugar comes back down to the 100s at two or three hours after eating, making them look "mild" on an oral glucose tolerance test or fasting glucose screen but those post meal spikes are high enough to cause damage, especially to the vagus nerve which controls vital functions like heart beat and blood pressure.

In addition, in the side of our family that carries the "mild" diabetes gene, there is a very high prevalence of severe disc problems. I have one that has really limited what I can do since my discs have ruptured. My dad had this as did several uncles. Only recently did I learn that specialists now think these disc problems may be caused by blood sugar problems that affect the blood supply to the disc tissues, weakening them.

This isn't a fatal complication, but the months my one uncle spent in excruciating pain in a full body cast didn't do much for his quality of life, and I'm not thrilled with the limitations that my disc injuries place on my doing just about anything I'd like to do be it swimming or carrying my own suitcase!

Knowing what I know now, I wonder if treating my "mild" elevated blood sugars more aggressively when they were first noticed in my 20s might have kept me from developing the disc problems later on. I was fortunate to get a relatively early diagnosis when my blood sugars started surging into the mid 200s and I adopted a policy of striving for normal blood sugars which probably prevented worse things from happening, but that only happened because I read widely and refused to accept my doctor's assurances that mid-200 mg/dl blood sugars after meals were "nothing to worry about" because my fasting blood sugar was "only" 108 mg/dl.

So my advice is this: If you are told you have a "mild" form of diabetes don't think this means you can ignore it. take it seriously. Yes, you are much more fortunate than people who have severe forms like Type 1. But if you neglect your "mild" diabetes your absence of "classic" complications might not mean much since ignoring high blood sugars after meals might just give you a fatal heart attack.

And my grandmother on the side of the family that carried the gene did die of diabetic kidney disease in her early 70s, which suggests to me that no matter how "mild" your diabetes may be, if you live long enough it will eventually cause microvascular complications.

BOTTOM LINE: No matter how "mild" your diabetes might be, go for completely normal blood sugars to ensure completely normal health!

October 3, 2007

Study: The So-Called Glycemic Index is Nonsense for Type 2s!

Diabetes In Control points today to a study published in Diabetes Care that proves what I've been saying for years.

The Glycemic Index is meaningless for people With Type 2 Diabetes.

Interindividual Variability and Intra-Individual Reproducibility of Glycemic Index Values for Commercial White Bread

The glycemic index is a measure of the impact a food has on blood sugar. The study found that while the average glycemic index of white bread was 71, in the individuals who participated in the study the actual glycemic response could be anything from 44 to 132. In short, it was meaningless.

This is no surprise. As I wrote in an earlier blog entry, The "glycemic index" is meaningless for people with diabetes because all that supposedly "high glycemic" foods do is slow down the digestion of the carbohydrates they contain.

If you have enough phase two insulin to mop up carbs 2 or 3 hours after eating, a slower digesting high carb food will be a bit better for your blood sugar. But most people with longstanding Type 2 diabetes have little or no second phase insulin. So it doesn't matter how long it takes a food to digest. Every gram of carb they eat will hit their blood sugar and raise it. For them, it doesn't matter if they're eating Oatmeal or drinking regular Pepsi, 50 grams of carbs in either form will push up their blood sugar to damaging levels.

If you don't understand what "second phase insulin response" is, read this page: How Blood Sugar Control Deteriorates. It will explain a lot of things your doctor forgot to mention--or doesn't know.

Because there is so much individual variation in response to a given amount of carbohydrate, the only way you can decide what foods make a healthy diabetes diet--FOR YOU--is to test each food you eat with your meter. If the food keeps you at a healthy blood sugar target, which, at a minimum should be under 140 mg/dl at 1 hour and under 120 mg/dl at 2 hours, eat it. If it doesn't, cross it off your list.

The main reason you've heard so much about the so-called glycemic index, is that it allows makers of high carb foods to market their damaging wares to people with diabetes as "health food." When the ADA chimes in with their magazines full of supposedly "healthy" very high carbohydrate pasta and oatmeal recipes, you can see how effective this marketing strategy is.

Too bad it causes blindness, amputation, kidney failure and heart attack death. But marketers (and the ADA) don't seem to worry about that kind of thing.

The one thing that has me scratching my head here, is this. Why is it that I could figure out years ago that the Glycemic Index was nonsense when PhDs and MDs can't. Do these people know anything about the physiology of diabetes beyond the "facts" that drug company salespeople, many recruited--I kid you not--from Big 10 Cheerleading squads--have told them?

October 1, 2007

Trans fat -- Lying Labels!

On my last trip to the grocery store, I spent some time examining labels to see how manufacturers have dealt with the requirement to report trans fat on the labels.

The news is not good. As far as I can tell, most commercial baked goods and many other products still list hydrogenated fats and oils early in the list of ingredients, which means there is a significant amount of trans fat in the product no matter what the labels say.

In most products--with a few exceptions--the hydrogenated fats they used to contain have not been replaced with other kinds of fats and oils. Even so, just about every product you pick up that lists hydrogenated fats and oils in the ingredients also provides a nutrition panel that claims there is 0 trans fat in the product.

How can this be? There are several explanations.

  1. Manufacturers are allowed to round down, so they may have .5 grams of trans fat in a serving and report it as 0.

  2. Manufacturers use unrealistically low portion sizes. If you weigh out a portion of many common foods you'll find that the portion you would have served yourself is often a lot more than what is used as a portion on the label. This magnifies the impact of that rounding as your true life portion that is three times as high as the label portion may have 1.5 grams of unreported trans fat.

  3. Labels lie. No, this is not me being paranoid. Over the decades I've been following nutrition news several newspapers have paid to have labs analyze commercial prepared foods and compare the lab results with the actual contents of the package.

    In the early 1990s, the Hartford Courant analyzed ice cream and found that the calories listed on labels bore no relationship to the truth and that there were often 50 calories or more in a serving. To make it worse, the portion size for ice cream is unrealistically low. Try measuring a serving by weight (not volume, which is deceptive) and you'll see what I mean. As a result the typical scoop of ice cream serving was found to have at least 100 calories more than what the labels would suggest.

    More recently, in the late 90s, a Florida newspaper analyzed low carb foods and found that they almost all contained many more grams of carbohydrate than were reported on the labels.

There is No Enforcement of Truth in Labeling and No Real Punishment for Companies That Lie on Labels

It's a lot easier to remove the trans fats from a label than from the food itself.

The underfunded, understaffed FDA can't even keep up with the poisoned foods entering our food supply, so you can be sure it is not putting any resources into testing tens of thousands of packaged food items to see if the nutritional information on the package matches what is inside.

Even more to the point, in the very few cases where a company has been found to be lying on labels--by others, not the FDA--the punishment is a joke. The Atkins Nutritionals company, for example, was forced to settle with consumers who bought its mislabeled bars. But in order to file a claim the consumer had to have proof of purchase (of a bar bought months before!) and if they did, the settlement merely sent them coupons to be used for buying more product from the company!

Why Should You Care?

Remember all the hoopla about how dangerous saturated fats were? Well, it turns out many of the early studies that looked at the relationship of saturated fats and heart disease did not separate out trans fats from saturated fats. And it turns out that it is trans fats that are the really damaging fats that clog up arteries. They raise LDL, lower HDL, and also raise triglycerides.

For people with diabetes the stakes are even higher since those without normal blood sugars are more at risk for heart disease already, as high blood sugars also raise LDL, lower HDL, and raise trigycerides. So for anyone with diabetes of any kind avoiding trans fat should be a priority.

How Can You Protect Yourself Against Lying Labels?

Read the ingredients, not the nutritional panel.

If you see the word "hydrogenated", assume that the product contains more trans fat than the label discloses and far more than is healthy for your body.

One legal trick companies resort to is to list fats like this: "sunflower oil, soybean oil, or partially hydrogenated vegetable oil." This means that the company can use any one of the listed ingredients. In practice it means that they are using the cheapest (usually the hydrogenated oils) but listing ingredients in this way suggests to the consumer that the product contains the better quality oils listed first.

Don't be fooled. There is no amount of trans fat that is good for you. All of it is bad and you should let manufacturers know you care by avoiding buying any products that contain them.