What's the Best Diabetes Diet?

Easy question! The best diabetes diet is the diet that keeps your blood sugars within the normal range after every meal.

What foods you eat to achieve this goal will vary greatly since your own personal blood sugar response to food varies depending on a lot of factors. For almost all Type 2s it is the carbohydrate in their foods--both sugar and starches--that raises blood sugar. What varies is how high and how fast those blood sugars rise in response to carbohydrate in the meal.

Factors Affecting Your Tolerance for Carbohydrate

• Your Weight. Many people don't realize this, but the amount that a gram of carbohydrate will raise your blood sugar depends on your size. If you are 300 lbs, you'll get 1/2 of the rise in blood sugar from that gram of carbohydrate as would a person who weighs 150 lbs. This is one reason why the "one size fits all" recommendations for how much carbohydrate you should eat are deeply flawed.
  
  
• What Physiological Problem Causes Your Diabetes. There are many different physiological problems that cause Type 2 diabetes and different causes can give you a very different response to the carbohydrates in your meals.
  
  That is why you have to test the different foods you eat to find out whether they fit on your own, personal, diabetes diet. What works for one person may fail miserably for others.
  
  Most notoriously, the supposed "low glycemic" foods and "healthy whole grains" recommended so heartily by people who don't have diabetes can raise your blood sugar very dramatically if you don't have a strong phase 2 insulin response.
  
  If this term isn't one you are familiar with, you can learn about the phases of insulin response HERE.
  
  If you do still have a strong second phase insulin response, which some Type 2s do, you will be able to eat these slower carbs. If not, they'll cause blood sugar spikes every bit as damaging as those from supposedly "faster" carbs.
  
  
• Your Meds. People have very different responses to every diabetes medication, again because the underlying cause for their abnormal blood sugars can vary so widely.
  
  For me, without any meds, eating 60 grams of carbohydrate would reliably put my blood sugar at 250 mg/dl or more at one hour after eating. With Metformin alone, that would drop to maybe 200 mg/dl, with metformin and 3 units of insulin, it would drop to about 140, maybe less, but I'll end up in the 80s at 2 to 3 hours later making it a bad idea for me to use any more insulin--or eat any more carbohydrate. With Januvia my blood sugar would rise to 129 mg/dl and then start dropping, though because of my concerns about the side effects, discussed elsewhere I avoid Januvia for now.
  
  Thus you can see that my "diabetes diet" is going to be different depending on what meds I'm taking. Yours will be, too.
  

It is because people vary so much in what their own bodies can tolerate that you see the vicious online "diet wars" where people who can eat a lot of carbohydrate accuse those who can't of being fanatics, and those who can't accuse those who can of living in a dream world. Throw in dietitians and doctors who have never tested their own blood sugar in response to food intake and know only what they've read about nutrition in studies, often conducted among people who do not have diabetes and you can see why diet becomes an area fraught with myth and controversy.

That's why the only way you can find out what your own diabetes diet should be is by using your meter and testing the foods you eat--starting out with the understanding, that there is going to be a limit on how much starch or sugar every person with Type 2 diabetes can handle. If you could eat all the sugar and starch you wanted and get normal blood sugar readings, you wouldn't be diabetic, would you?

Straight Talk about Safe Blood Sugar Targets

There's a huge difference between truly safe, normal, blood sugar levels and the blood sugar levels too many doctors and diabetes educators tell you are "okay for a diabetic." This is because the ADA has, for years, told people with diabetes that they should settle for dangerously high blood sugars so as to avoid hypos.

Since Type 2s controlling their diabetes with diet alone are incapable of experiencing dangerous hypos, this is flawed advice. Type 2s taking all oral drugs except for Sulonylureas like Amaryl and Glipizide are also incapable of experiencing dangerous hypos.

When you are not taking insulin or a sulfonylurea drug, feeling a bit shaky as your blood sugar gets to a normal level--anything 70 mg/dl (3.8 mg/dl) or higher--is not an actual, damaging hypo, just a sign that your body isn't used to normal blood sugars. That kind of "hypo" feeling will go away as your get used to normal blood sugars.

This means that there is NO reason for you to avoid shooting for truly normal numbers if you are a type 2 not sulfonylurea drugs. If you are on these drugs, you may have to talk to your doctor about reducing the dose as you bring your carb intake down to the level that gives you normal blood sugars.

Even Type 2s using insulin can shoot for these normal numbers, too, if they are taught how to adjust their doses correctly. A study presented at this past week's ADA conference found that patients instructed properly can adjust insulin levels better than their doctors. Read about it HERE.

I shoot for normal numbers with mealtime insulin and and I know plenty of others who do, too. Type 2s on insulin usually do not have the same problems with dramatic swings in blood sugar that Type 1s have, but many doctors do not realize this. (We'll discuss how to make sure your doctor is teaching you the most modern techniques of insulin dosing for type 2s in a future posting.)

What Blood Sugar Levels Should You Aim For?

I'd suggest aiming for blood sugar levels low enough not to damage your organs!

You can learn what science has found out about normal blood sugars HERE. You can read some of the better research that connects blood sugar levels with organ damage HERE

I'd suggest you start out by shooting for the following blood sugars after meals:

• One hour after eating: Under 140 mg/dl (7.8 mmol/L)
  
• Two hours after eating: Under 120 mg/dl (6.7 mmol/L)
  

Lower is better, but these are a great level to start with.

Don't obsess about whether you should count from when you start eating or afterwards. There's a natural variation in when the peak will occur but fifteen minutes in either direction won't make a significant difference in your health.

With some foods, like pasta or pizza that take a very long time to digest (or if your stomach for some reason doesn't empty at a normal rate) you might want to look at your blood sugars a few hours after these suggested times as the blood sugar peaks may be postponed.

There are going to be plenty of times when you don't hit these targets. Don't panic, just by attempting to hit them, you are making huge improvements in your health. And if you can hit them more than you miss you'll see a dramatic improvement in not only your A1c but in any early diabetic complications you might have picked up, most notably neuropathy.

NOTE: I've written a longer piece explaining some of the tips and tricks that can help you make a diabetes diet work over the longterm on this page:A Diabetes Diet is Different from a Weight Loss Diet

$33K Average Pharma Payment to VT Endos

[NOTE: This blog entry appeared in a different form earlier, but a concerned friend who, unlike me, gets paid to write about diabetes, feared that the wording might cause drug companies to sue me. I have therefore rewritten it in such a way that should preserve my modest assets from drug company legal attack.]

It's no secret that doctors often prescribe the newest, most expensive drugs and medical devices to patients when there are often older, better-tested drugs and devices that would do the same or even a better job. One reason for this is that drug and device companies provide huge financial incentives to doctors who prescribe their expensive new drugs and devices.

How big are those financial incentives? An article in today's Now the New York Times gives you a clue. The Times reporters sifted through mandatory reports from the very few states where Big Pharma is legally required to document their "marketing expenditures" to doctors.

One of these states is Vermont, a state with a tiny population and few doctors or hospitals. There are only 11 endocrinologist listed in the yellowpages.com listing for all of Vermont. Though this listing probably misses a few, I'd be surprised if there are more than 30 board certified endos in the whole state.

The New York Times reports that in Vermont Big Pharma paid the top five endocrinologists in Vermont an average of $33,730 each.

This is not counting the cost of free drug samples or the salaries of marketing reps." The reason they only reported what they paid those "top" five endos is this: the law only made the drug companies list the top 100 doctors they made payments to and there were only five endocrinologists on this list. Even so, the median cash amount paid these endocrinologists was the second highest of that paid all specialists. Only the psychiatrists earned more.

For comparison purposes, the per capita income in Vermont in 2006 was $34,264, a mere $534 more than the average amount that Big Pharma paid each top Endocrinologist.

What exactly was Big Pharma paying these doctor for?

The reports do not answer this, but I can tell you from personal experience what some of these payments might have been about. My doctor also has an office in Vermont (the border is only some 10 miles away from my home). Recently she has been signing up patients for a "study" run by a large pump manufacturer. The study involves having patients wear a CMGS for a brief period. The patient cannot see the CMGS display during this trial, but when they return the CGMS the company downloads the information and presents it to the doctor.

I was in my endo's waiting room one day when the chirpy pump company rep was talking with the office manager. I wasn't eavesdropping. This conversation was conducted in the middle of the waiting room at normal conversational volume. I knew this was a pump saleslady, because earlier she'd been sitting right next to me, in the same waiting room, enthusiastically pitching her company's new pump to one of my doctor's patients who, the conversation revealed, already was using another company's (less expensive) pump. She had signed him up for the new pump by the end of the conversation.

The conversation with the Office Manager went like this: Pump Saleslady: "Here's the printout of X's readings. He really needs a pump." Office manager. "Oh, yes!"

The cost of the pump this rep was selling is about $9,500 (much higher than that of competitors) with ongoing monthly costs of several hundred dollars more--which add another ten thousand bucks to the cost of the pump over three years. This "study" very conveniently identifies new customers for the pump--ones whose blood sugars are bad enough that the company will be able to get the insurer to spring for it.

If you believe this study was being done for some more altruistic, research aim, well, I hope you enjoy your visits from the Tooth Fairy.

But after overhearing this exchange, I wondered how much the pump company paid my doctor to participate in this "study" which was so helpful in identifying new customers for their pump product.

Paying doctors to participate in "studies" meant to sell product is a common method that drug companies use to push their products. A spate of reports in the press suggest other ways that the drug companies distribute that money to doctors. They often pay doctors to enroll patients in questionable clinical trials--even signing up doctors who have been censured for killing too many patients or who have been denied hospital privileges for unethical conduct.

After Sanctions Doctors Get Drug Company Pay - New York Times

Drug companies also slip money to doctors via various sleazy "charities" the doctors set up for themselves.

Charities tied to doctors get drug company gifts - New York Times

Another study, this one published in the New England Journal of Medicine queried doctors about the money they received from drug companies and reported that according to the doctors themselves:

• 83% of physicians received food and beverages from pharmaceutical company sales representatives;
  
• 35% received reimbursement for the cost of attendance at continuing medical education conferences sponsored by pharmaceutical companies; [These conferences are often thinly disguised marketing pitches for the drug company's newest, most expensive drugs, not unbiased educational events]
  
• 28% received fees from the pharmaceutical companies for consulting, speaking engagements or enrollment of patients in clinical trials;
  
• 7% received tickets to sports events and entertainment
  

Statistics taken from: A National Survey of Physician–Industry Relationships

As was the case with the study I observed in my doctor's waiting room, often the "studies" that drug companies pay doctor for involve getting patients to use drugs or devices already on the market, and these "Study," rarely comes up with any result that gets published in a peer reviewed journal.The doctor's payment for participating in the "study" depends on the number of patients they have signed up.

Though the patient may be given a free sample for the rudimentary "study", the idea is that they will keep taking the expensive new drug or buy the device after the very brief "study" is over, when, of course, the cost of continuing the drug or device is paid for by the patient or the patient's insurer.

Lovers of the free market contend that this is how capitalism works. But my question to you--including all you investors who have been visiting this page in droves of late--is this:

If you or a loved one were ill, which would you want: The drug that has been proven to work well for your condition which is reasonably priced and has a ten year safety record, or a brand new drug, rushed through the approval process, which costs 16 times as much as the other drug and whose side effects--some of them fatal--won't become known for another seven years?

And if your doctor were prescribing the more expensive drug for you--one which might kill you because its maker had avoided funding studies that would reveal its flaws--solely because that doctor was being compensated for writing that prescription, would you still be such a fan of the free market?

This isn't a hypothetical question. It's happening every day. And if you making money investing in one of these drug companies, you really should stop and do a reality check and ask yourself, if these drugs are so wonderful, why does the drug company have to pay doctors the equivalent of a years' income to encourage them to prescribe them?

Study REALLY Proves Byetta Sucks for Most Type 2s

UPDATE (April 2, 2013): Before you take Byetta, Victoza, Onglyza, or Januvia please read about the new research that shows that they, and probably all incretin drugs, cause severely abnormal cell growth in the pancreas and precancerous tumors. You'll find that information HERE.

Original Post:

If you read title, this study sounds like it proved that Byetta is great for people with Type 2 diabetes--and that's how the press is playing it.

BYETTA(R) Study Showed Sustained Blood Glucose Control Over Three Years in People with Type 2 Diabetes

But read further and you'll see how sad the results of this study really were.

Byetta Produced Dangerous Blood Sugar Levels in 70% of those taking it.

The press release brags:

"After three years of BYETTA treatment, 46 percent of study participants achieved the American Diabetes Association's recommended target A1C of 7 percent and 30 percent
of participants achieved an A1C of 6.5 percent." [emphasis mine]

This means that fully 7 out of 10 of those taking Byetta had blood sugars high enough to damage their organs for the full 3 years of the study.

The American Association of Clinical Endocrinologists' (AACE) target of 6.5% which these people did NOT attain is the minimal level at which people with Type 2 diabetes are less likely to develop retinopathy, kidney failure and nerve death leading to amputation. And the 6.5% A1c isn't ideal, as it still represents a higher risk for heart disease than a 5% A1c would be.

The ADA's 7% A1c target is helpful for people with Type 1 diabetes, but the major study of people with Type 2 diabetes, the UKPDS, found that maintaining a 7% A1c only reduced microvascular complications in Type 2s by 12% far, far less than it did for Type 1s. In short, it's dangerously high for a Type 2.

So what this study really says is that seven out of ten people in this group of patients, despite taking a very expensive injectable drug for three years, maintained blood sugars high enough to damage all their organs over a three year period.

And this is supposed to be good news.

It gets worse.

Byetta Caused Trivial Weight Loss in Most People

When patients report that Byetta isn't helping their blood sugars, they are told to keep taking it because it causes weight loss.

But here's what Lilly's own press release claims their own study found about Byetta's weight loss.

"Weight loss from baseline was progressive, with participants losing on average 11.68 +/- 0.88 lbs at three years. In addition, one in four patients lost an average
of 28.66 lbs."

What this means is that three out of four people taking this expensive drug that did NOT control their blood sugar lost an average of 11.68 pounds over three years, or not quite four pounds a year.

This, in a population of obese Type 2s who typically weigh 250 lbs or more. You tell me, is this a dream weight loss drug? Or are patients being had?

Now it is true that one out of four of those in the study lost an average of 29 lbs over 3 years, which is better than the three quarters who got almost no results, but people who adopt low carb diets usually lose at least that much, too, and they do it without expensive drugs and with far better blood sugar control.

I lost about 29 lbs myself over a one-year stint of low carbing in 2002 and I have kept it off for 4 years even after raising my carb intke--which is documented in my participation in the longterm CCARBS study where I had to be weighed every year by a doctor.

So here's the truth about Byetta:

Byetta is Magic for a Few and a Dangerous Distraction for the Rest of Us

We've all heard the success stories, most notably that of David Mendosa who is bragging about his huge weight loss and reversion to normal blood sugars all over the web. But this study makes it crystal clear that Mendosa is one of the very few, very lucky people who have something wrong with them that Byetta can fix.

You'd have to be delusional to believe that Medosa's experience is not the exception, rather than the rule. Lilly's own data, summarized here, suggests and that spending a few years on Byetta may give your high blood sugars the chance they need to make you go blind, kill your nerves, and put you on dialysis.

Bottom line: There's no harm in trying Byetta. Maybe you'll be one of the very few lucky folks for whom it is a magic elixir. But if you don't have normal blood sugars after 6 months on Byetta--as defined by a 5% A1c or better, demand your doctor put you on insulin to normalize your blood sugars and assure your health. Staying on this drug for years while your A1c is over 6.5% month in and month out makes as much sense as playing Russian Roulette.

When it comes to blood sugar control, there is only one drug that ALWAYS works: Insulin, when dosed correctly.

And if your doctor tells you that Byetta is a great drug, ask him how many of the patients he is treating with it have A1cs below 6.5% or 7%. If the answer isn't, "Most", it's time to find a better doctor.

Thin Type 2s Disprove that Obesity Causes Diabetes

If you get your medical information from the press, you probably believe that Type 2 diabetes is a self-inflected disease caused by obesity and that it could have been prevented if the lazy gluttons who get it had only watched their weight.

This makes it very easy to view people with Type 2 as greedy layabouts who caused their disease and to begrudge them their share of society's limited health care dollars.

People with Type 1 often express their anger and resentment that they have to share the name of their disease with all those lazy fat people, when the Type 1s disease is not their fault.

But the theory that Type 2s are greedy slobs who cause their disease, though appealing to our prejudices, is crap.

There are many thousands of people who have been diagnosed as Type 2s who are not fat. Last year I attended a get together of a bunch of us who met by posting on an online bulletin board. What we had in common, besides a Type 2 diabetes diagnosis--which is what my doctor still puts on my paperwork--is that we were all of normal weight. There were quite a few overweight people in the cafe with us the afternoon we met, but they weren't the diagnosed diabetics.

And more importantly, despite attaining normal weights, all of us who met that day still have seriously impaired blood sugar. Two of us, in fact, use insulin to get better control.

Part of the reason for the association of diabetes with obesity is that people with diabetes often are very fat. But what gets missed is that their obesity often develops as a result of the very high blood sugars, rather than the other way around.

We know now that blood sugars of 180 mg/dl or higher cause insulin resistance and there appears to be a strong relationship between insulin resistance and the tendency to pack on weight. So when people's post-meal blood sugar control starts to deteriorate one of the first things that happens is that they pack on extra pounds.

This relentless weight gain often happens during the ten years or so that the typical Type 2 is running diabetic blood sugars after every meal but before they get a diagnosis--the same ten years of undiagnosed high blood sugars that ensure that at the time of diagnosis almost half of all "newly diagnosed" Type 2s already have serious diabetic complications, including nerve damage, retinal changes, and early signs of kidney deterioration which take a decade to develop.

Hence, for many type 2s, that overweight that doctors think has caused their diabetes is really just another complication caused by their years of exposure to high blood sugars. Even more important, this weight gain can often be reversed by cutting out the carbohydrates that raise blood sugar, though resuming normal weight rarely results in our diabetes reversing.

Another fact that gets lost when the media, and even doctors, blame people for their diabetes is this: that only a small proportion of even the most obese people ever develop diabetes--something like 1/3 of them. The rest just end up very fat with normal or near normal blood sugars.

That is because a huge body of research has shown that people only develop diabetes when they have underlying genetic conditions that are not well understood, but which are clearly there, since twin studies show a high concordance for diabetes. Even more interestingly, studies of thin relatives of people with type 2 diabetes show that they show subtle blood sugar abnormalities while they are thin and fit--decades before they themselves are diagnosed with Type 2 diabetes.

I have written up some of the more interesting research on this topic on my page:

You Did NOT Eat Your Way to Diabetes

Quite a few people diagnosed with Type 2 diabetes have written to me that this page saved their sanity after diagnosis. Even more have written to me of their anger at doctors who had told them that, if they could just lose ten pounds, their diabetes would reverse when they were at normal weights already.

Similarly, it seems like almost every week I get emails from people who have been diagnosed with Type 2 diabetes who are not fat, but whose doctors are so sure that diabetes is caused by obesity that they can't even take in the evidence of their own eyes.

Even worse, a lot of people, like myself, go for years--in my case 13 of them--without a diabetes diagnosis because doctors take one look at their size 8 slacks and say, "You couldn't have diabetes, you are thin," despite the presence of classic tell tale symptoms like UTIs, yeast infections, fluctuations in vision, exhaustion after eating carbs, and in my case, gestational diabetes during not one but two pregnancies.

I thought for years my situation was unique, but the mail I get makes it clear it is not.

Unfortunately, the media will write up with enthusiasm stories of hugely overweight people who reversed their Type 2 diabetes by losing weight. Some of these people do exist, though in my experience of reading about the experiences of literally thousands of people with Type 2 diabetes online, the people who do this are almost always male. But they are not typical of all Type 2s at all.

It is a shame that the media will not describe the stories of people like me who exercised, kept slim, and developed diabetes anyway. I wish they would. Any journalist who would like it interview me can click on the link by my profile above. Just promise you'll be willing to photograph me in my size 8 pants injecting insulin.

Januvia and Melanoma

UPDATE (April 2, 2013): Before you take Byetta, Victoza, Onglyza, or Januvia please read about the new research that shows that they, and probably all incretin drugs, cause severely abnormal cell growth in the pancreas and precancerous tumors. You'll find that information HERE.

Original Post:

Because this blog was one of the very first to discuss Januvia, I get a lot of visitors who find this site via a Google or Technorati search on the term "Januvia." So I thought I'd post a bit more about my major concern about this new drug.

Whatever it does for blood sugar, the big problem I see with Januvia is that the testing that the FDA required before they approved it for use did not look at what the other effects might be of its new and very powerful mechanism.

As a result, Januvia has gotten the undeserved reputation of having very few side effects. This has gotten a lot of doctors prescribing it, despite its cost, which is among the very highest for any diabetes pill, ever.

But the problem is that Januvia uses a new and not well-understood mechanism. It works by keeping an enzyme from being produced. This enzyme, DPP-4, stimulates the removal of another substance, GLP-1, from the body. Since GLP-1 can stimulate insulin release, allowing GLP-1 to build up can cause more insulin to be produced by the beta cells, lowering blood sugar.

That's good, and in a person who still has living beta cells that are capable of secreting more insulin than they do, DPP-4 inhibition lowers blood sugar, though the amount it will lower it depends on how insulin resistant the person is and how much excess capacity their beta cells have left.

But here's the problem: DPP-4 isn't just used to keep GLP-1 levels from building up. It is used throughout the body for many other functions, many of which involve the immune system and brain. Even more important, scientists do not yet fully understand these functions of DPP-4.

This means that they also don't know what the effect of inhibiting its action will be. And even more importantly, the testing that the FDA required of Merck before approving Januvia did not look into the effect of inhibiting this enzyme in other parts of the body.

This is not trivial. There are cancers, most notably melanoma, in which researchers have found that the cells become malignant when they stop producing DPP-4. When DPP-4 production is restored to these cells, they stop being malignant. That would suggest, at a minimum, that the testing for Januvia should have looked to see what the impact of artificial, drug-induced inhibition of DPP-4 would be on these particular kinds of cells and whether inhibiting DPP-4 for a long time would lead to more melanomas developing. This was not done.

The standard drug acceptance process involves using some standard cancer tests. But these tests do not involve looking at the effect of removing DPP-4 on the specific kind of cell that responds to DPP-4 suppression by turning cancerous. The cancer screens look for the ability of a drug to cause tumors in rats (which, by the way, Januvia did do at very high doses.) They look at the effects of a drug in a test tube culture to, to see if the drug messes up the DNA in a way that leads to cancer.

But what we are talking about here is a drug that doesn't cause cancer by messing up a cell's DNA. Instead, what it might do, is disable the enzyme the body uses to get rid of cancerous cells once some other mechanism has made them malignant.

With melanoma, the mechanism that turns cells cancerous is working on all of us--sunshine. But most of our bodies get rid of cancerous cells before they have a chance to grown into large invasive tumors. How they do this apparently involves the use of DPP-4--which is the substance Januvia inhibits. So you can see that the standard cancer testing should not reassure you that Januvia doesn't cause cancers to grow out of control.

This really worries me. Especially since so few people know about the relationship of DPP-4 and melanoma. I do, because I'm a melanoma survivor. And I can tell you right now that the reason you don't see people wearing "beat" melanoma ribbons, and going on melanoma runs, and painting and singing about how much they grew spiritually through fighting melanoma the way you do with breast cancer, is because most people who fought melanoma are dead.

Whenever I tell someone I have had two surgeries for melanoma they tell me about some relative or friend who had it, was told they'd be fine, and then died of it. I'm very lucky my melanoma was in a very visible spot and that a doctor saw it early enough for me to be able to have it removed before it had penetrated through the bottom layer of the skin and into my bloodstream. Once this happens, your chances of survival plummet.

Even though I'm supposed to be fine, I am not allowed to donate blood or organs because there is a good possibility that melanoma cells are floating around in my body which would seed themselves in the person who received my tissues and kill them.

That's how nasty melanoma is, and why it really troubles me that there have not been any specific studies to see what the effect of Januvia's form of DPP-4 inhibition is on melanocytes.

Januvia was approved after a very short trial--barely two years long--and melanoma can take quite a few years to develop to where anyone would notice a melanoma lesion and consider it abnormal. I had actually shown my lesion to a skin doctor 4 years before it was biopsied and found to be melanoma. But the first time I showed it to the skin doctor, he only inspected it visually and told me it was "nothing to worry about." It was about ten times larger by the time a doctor did consider it something to worry about. Before that, I foolishly assumed it was nothing because the skin doctor had told me that.

So unless every single suspicious patch of pigment on every participant in the Januvia trials was biopsied, we have no idea whether or not they had developed very early cell changes leading to melanoma during the brief, two year trial.

Even worse, there is a form of melanoma which develops inside the body, in melanocytes that live in the linings of organs, and which is only detected when it has spread throughout the body and created tumors large enough to be observed as large lumps. If study participants developed this kind of melanoma, it would only be detectible on full body CT scans, which, of course, they were not given.

When I first read up on this, I asked quite a few doctors about it, and they had no information about it at all. Then I started emailing the researchers who had published about Januvia and DPP-4 inhibition. Eventually one, (whose name I promised to keep private) told me that my concern was real and that the research simply has not been done to answer the question about the possible melanoma risk.

You can be sure, with the pills selling for $6 each, that Merck is not about to do that research any time soon. This is, after all, the company that suppressed the heart attack data on its drug, Vioxx, and which is now selling another drug that research shows is equally dangerous, Arcoxia, despite data that shows it kills tens of thousands of people who would have lived had they used Ibuprofen, a drug that works just as well as Arcoxia.

So if you are thinking of taking this drug, give it some serious thought. Is it really worth the risk Januvia represents to get a .5% lowering of your A1c? And if your doctor tells you there are no side effects, do ask the doctor what they know about the effect of DPP-4 on melanomas and why they are sure inhibiting DPP-4 with this drug is safe when no research has been done to look into this.

Type 2s: Insulin Early is Easy, Insulin Late is Not

I keep reading postings here and there on the web from people with Type 2 diabetes that say something like, "My A1c was 11.5% even with Metformin, so my doctor told me it was time to go on insulin."

It is postings like this that bring home to me why so many Type 2s develop terrible complications, and even more importantly, why even those who are taking insulin often have dangerously high blood sugars.

The most conservative of medical groups--the ADA--tells doctors that an A1c over 7% is going to cause serious diabetic complications like blindness and kidney failure. Yet these people's doctors have encouraged them to dick around with oral drugs when their A1cs were 10% or higher!

The years they've spent at those dangerously high blood sugar levels waiting for oral drugs to do what all the research evidence shows oral drugs cannot do have wreaked havoc on their organs that may not be completely reversible, no matter what their blood sugars might be in the future.

In fact, a recent survey I read somewhere on the web found that most family doctors don't put their patients on even an oral drug until the patient has spent a year with an A1c of 8% or higher. That is a whole, long year where dangerously high blood sugars are producing early retinopathy, advancing neuropathy, and making small changes that lead to kidney failure.

Since none of the oral drugs is capable of lowering A1c much more than 1%, this kind of treatment is criminal. A patient whose A1c is 11.5% on metformin probably started out with an A1c of 12% or even higher. If you don't believe me, go read the Prescribing Information for each of the common diabetes drugs. They show exactly what the median change in A1c is that their drugs can achieve, and you'll see it is rarely much more than a 1% drop in A1c. For a patient with a 12% A1c, even a 3% drop would be pitifully insufficient. But that is how these people's doctors are treating them.

All that unnecessary suffering. It makes me want to weep!

For patients with an A1c over 8.5% there are only two therapies that will reliably bring blood sugars into the safe zone. Let's look at them now, very carefully.

Carb Restriction

Many newly diagnosed Type 2s with surprisingly high A1cs have reported online that they have been able to bring their A1cs down from 10% or higher to the safe 5% range by cutting the carbohydrates out of their meals until they were able to get a blood sugar under 140 mg/dl at one hour and 120 mg/dl a two hours after eating.

Though doctors pay lip service to the idea that their patients can control diabetes with "diet" a depressingly high proportion of these doctors seem to think that "diet" means "weight loss diet" rather than "Carb control diet" so their patients end up starving on high carb/low fat meals that push up their blood sugars to levels guaranteed to destroy eyes, nerves and kidneys.

Cutting out the carbs that raise blood sugar is the only "diabetes" diet that will improve blood sugars for every person diagnosed with Type 2 diabetes. So for the newly diagnosed Type 2, or the Type 2 who has never tried cutting way back on their starch and sugar intake, a stint of eating a true diabetes diet, one that avoids all starchy foods, no matter how full of "whole grains" they might be, a diet made up almost entirely of healthy greens, cheese, lean meats, nuts, berries and nonstarchy vegetables may be all that is needed to perform blood sugar rescue.

But if cutting your carbs doesn't make a dramatic difference in your A1c within a few months, there is only one sane therapy to consider, and the faster you demand it, the less likely you are to end up as another tragic diabetes disaster story.

That therapy involves insulin.

Insulin

Unlike every other diabetes drug you may read about, insulin, prescribed properly (and those words are key) always works. Insulin is the only drug that will lower blood sugar in every critter that has a blood stream with glucose floating around in it. Rodent, fish, monkey, or you, insulin WILL lower the blood sugar. And insulin can lower blood sugar however much you need it lowered, if--and it is a big if--you learn how to use it correctly.

This is such a simple concept, you have to wonder why most doctors treat insulin like it was devil's blood, trying every other possible treatment--some of them quite dangerous--before putting their patients on the one treatment that is capable of giving them normal blood sugars.

In the past, doctors seem to have assumed that needles were so terrifying to patients that they would not use them unless faced with immanent death, and as a result, insulin wasn't prescribed until Type 2s were on death's doorstep. (Which, unfortunately, has made a new generation of diabetics assume that if you get prescribed insulin, you are on your way out.)

But look what happened when Big Pharma came up with a new treatment, Byetta, that was rumored to cause weight loss. Despite the fact that Byetta treatment requires not one but two needles a day and can cause projectile vomiting, patients lined up demanding it and thousands of Type 2s are happily injecting themselves and whoopsing their way to happiness. So clearly when patients perceive a benefit in a treatment, they'll put up with needles.

The benefit of insulin can be much greater, since Byetta only works to lower blood sugar significantly for a subset of those who take it. Insulin always works.

Insulin Early is Easy, Insulin Late is Hard

My belief--and this is how I treat my own diabetes--is that if diet (defined as cutting carbs) plus the one safe med, metformin, and possibly Byetta, don't give you normal blood sugars, it is time to move to insulin while the beta cells still have enough life in them to make insulin safe and easy to use.

This is a huge point many doctors miss. If your pancreas is a mess of scar tissue, you probably have lost your alpha cells too, and this means that you may have little or no ability to secrete glucagon to raise your blood sugar if it goes too low.

If, on the other hand, you start using insulin when you still have 20-30% of your beta cells living, you can use lower doses of insulin and if you take too much your body will push your blood sugar out of the hypo range, because it still has the other pancreas-produced hormone it needs to do so.

People with no beta cells have a much tougher time using insulin, especially when they use it to control post-meal blood sugars. The stories you hear from Type 1s who veer from 35 to 350 mg/dl in a few hours give you some idea of what it can be like to use insulin when you have a dead pancreas.

But most Type 2s don't have a dead pancreas, and though only a few of us have pioneered the "insulin early, not insulin late" strategy, those of us who have find that it makes living with diabetes far easier than we ever thought possible. Insulin supplementation takes the burden off our struggling beta cells. It can let us fine tune our blood sugars to where they stay relatively flat and do not ever go near the zone where glucose floods into nerves, eyes, and clogs up tiny kidney filtration units.

As Dr. Bernstein points out, small inputs make for small mistakes, and when a Type 2 starts insulin early, the doses are much smaller than later, when they have no beta cells, and the mistakes are much smaller too.

Here are some things your doctor might tell you if you want to start insulin that you might want to question.

Insulin Myths

1. You'll gain weight.

This is what kept me from starting insulin for years, when I should have been on it all along. It turned out NOT to be true as long as I use insulin in a way that matches my carbohydrate input.

If you take more insulin than you need, you will get hungry. "Feeding the insulin" will pack weight on you. But if you learn how to determine your "insulin/carb" ratio, and inject an amount of insulin that matches your food, you should not gain weight. If you are taking a basal insulin, Levemir is also reputed to avoid weight gain.

And I also find that for me, the analog insulins seem to provoke hunger. But R insulin (the cheap kind) does not, and I even managed to lose a couple pounds last year while injecting R insulin 3 times a day.

2. You'll have hypos.

Using insulin requires using your brain. If you just want the doctor to tell you how many units to inject, and blindly do whatever you are told, hypos are a possibility.

But if you read up on how to use insulin--using the books and materials intended for Type 1s who, unlike Type 2s, get training in how to use insulin properly, you won't. I have not had a blood sugar reading under 60 mg/dl fifteen months of using insulin with my meals.

3. Needles are Painful

The shots don't hurt. I was as needlephobic as anyone, but it took about a day to figure out that my lancet for testing my blood sugar is a lot more painful than the hair thin needles I use for injecting. The first time I stuck myself with one, it was so painless I had to look down to make sure I really had stuck myself!

Right now one company is marketing an inhalable insulin, one that isn't very easy to use and which is very tough to match to carbs, by playing on people's fears of needles. It is much more expensive than even the most expensive injectibles, and it may harm the lungs. It is completely unnecessary.

Give yourself a few days to get over your needle phobia, and you'll end up laughing at how huge it used to loom in your mind. Injecting insulin really is No Big Deal.

4. All you need is one shot of basal insulin

There are two kinds of insulin. One lowers your fasting blood sugar and runs slowly in the background. Lantus, Levemir, and to a lesser extent NPH insulin are in this category. This kind of insulin does NOT bring down high post-meal blood sugars, it just lowers the point from which the post-meal spike begins.

Most Type 2s get put on basal insulin, because it is easy to use. But if your diabetes is mostly about very high post-meal blood sugars, a basal may not solve your problems. So you may think that insulin doesn't work for you, when in fact, the problem is you are using the wrong kind of insulin.

The meal-time insulin or "bolus" insulin is the insulin you match to your carb intake. The key for a Type 2 to making meal-time insulin work well is to keep your carb intake reasonable. Type 2s still have a small bit of homemade stuff that kicks in after a few hours, unlike a Type 1. It is not realistic to think you can eat 100 grams of carbs and match it with insulin, because the variations in timing of all that carb hitting your system, mixed up with your "sputtering pancreas" occasionally throwing a dollop of the homemade stuff, are too complex to calculate. And if you dump huge amounts of insulin into your system and it misses those huge amounts of carbohdyrate, well, yes, you do have a problem--one that can, worst case, put you in the ER.

But most people with Type 2 can match 30 grams of carb or even 40 with insulin without problems, especially after some practice, and possibly by using the slower R insulin which is more gradual in its effect.

It may take you a lot of cautious experimentation to figure out exactly how much carb and insulin you can use safely--starting out with a very low dose and a small amount of carbs and carefully adjusting carbs and insulin until you reach a level you can live with that gives you blood sugars that are safe and normal.

When Is Insulin NOT Useful

The only people for whom insulin is not a good idea are those who are still producing high levels of insulin, whose diabetes is caused entirely by insulin resistance, not beta cell failure. Many of these people are very, very large.

Typically, if your diabetes is caused by insulin resistance, your blood sugar will drop to normal levels very quickly as soon as you cut out most carbs. By "normal" I mean fasting blood sugars in the 80s or better. But if your diabetes is caused by beta cell problems, though your blood sugar will drop in response to a low carb diet, your fasting blood sugar may still be over 100 or worse no matter how low your carbohydrate intake.

You may also be able to determine if you are highly insulin resistant by having your insulin levels tested. If they are much higher than normal while fasting, then you may be seriously insulin resistant and adding insulin may not be the answer for you since your problem is that your body isn't using insulin, not that you don't have enough.

Doctors often seem to believe that all Type 2s are seriously insulin resistant, but in practice, this turns out not to be true. Mine told me I "obviously" was insulin resistant, but when I finally started taking insulin, my response was that of a Type 1 not a Type 2, showing I had very little insulin resistance at all--and that I really needed insulin supplementation.

That's enough for now. We'll come back to this topic again, though!

New "What They Don't Tell You" Summary Page

My Web Site, What They Don't Tell You About Diabetes has grown over the past three years to where it contains an entire book's worth of information--a full 85,000 words.

The downside of this is that the amount of information on the site can be overwhelming to new visitors. So I've put together a new introductory page which sums up the message of the site and helps the visitor decide which pages they want to visit.

Here's what I've come up with. If you have any comments or suggestions for improvement please let me hear them:

THE NEW SITE INTRO:

You Can Avoid Deterioration and Complications No Matter How Bad Your Blood Sugar is Right Now

• Type 2 diabetes does not have to be a progressive disease. Doctors think it is progressive because they don't recommend blood sugar targets that are low enough to prevent deterioration.

  Do People with Type 2 Always Deteriorate?
  How Blood Sugar Control Deteriorates
  From Normal to Type 2
  

• Prolonged exposure to blood sugars over 140 mg/dl (7.8 mmol/l) damages your organs and causes diabetic complications.

  Research Connecting Organ Damage to Blood Sugar Levels
  Healthy Blood Sugar Targets

• No matter how bad your blood sugar right now, you can get it down to a safe level.
  

  Inspiring Stories of People Who Did
  

• The way you get your blood sugar down is to do the following:
  • Cut back on your carbohydrates. Carbohydrates are the main thing that raises blood sugar. Replace starch and sugar with protein and non-trans fat.

    How to Get Your Blood Sugar Under Control
    A Diabetes Diet is Different from a Weight Loss Diet

  • If cutting your carbohydrates down to about 15 grams a meal doesn't give you normal blood sugars, ask your doctor to prescribe Metformin ER.

    The Truth about Oral Drugs - From Research
    Oral Drugs--A Quick Summary
    Be Safe with Rx Drugs
    

  • If Metformin ER doesn't help or isn't appropriate, try Byetta for a short time and continue using it only if you get strong results.

    Byetta and Januvia
    

  • If you still don't have normal blood sugars talk to your doctor about adding basal insulin. If basal insulin doesn't give you normal blood sugars, use insulin after meals too. Used properly with a lower carb intake, insulin will always work. If it isn't working for you, you need to find a doctor who can help you fine tune your dose.
    

    Insulin for Type 2 Diabetes
    

• Lowering blood sugars to normal levels can reverse some diabetic complications, most notably nerve pain (neuropathy) and early kidney changes.

  Neuropathy
  Diabetic Kidney Disease

• Diabetes is not caused by gluttony and laziness. Research shows it is a genetic disease caused by many different genetic flaws.

  You Did Not Eat Your Way to Diabetes
  

• Diabetes is often Not Diagnosed Correctly and Undiagnosed Diabetes Causes Complications

  • Not all Type 2s are overweight or insulin resistant. Those who don't fit this stereotype often fail to get diagnosed until diabetes has had years to ravage their bodies, especially those with very high post meal blood sugars and near normal fasting blood sugars.

    MODY

  • To determine if you have diabetes, you should test your 1 and 2 hour post-meal blood sugars. If your doctor tests you, make sure he orders a post-meal test, too. The Fasting Plasma Glucose test most doctors use often fails to diagnose diabetes especially in women.

    Am I Diabetic?

  • Many "diabetic" complications begin at blood sugars that the American Diabetes Association does not currently define as "diabetic"

    Misdiagnosis by Design - The Story Behind the ADA Diagnostic Criteria

There are many more topics covered on this site, but these are the ones that are most important. I invite you to come and read the whole site when you have time. The information you find here could save your health!

R Insulin - Cheap, Effective, and Unknown

If you are injecting meal-time insulin, you're probably using one of the analog insulins: Humalog or Novolog. Your doctor probably told you these are the newest, fastest insulins, and that is true. What he probably didn't tell you because few doctors know this, is that regular human insulin (R insulin) can be a better choice for many type 2s.

The reason your doctor doesn't know this has a lot to do with price. A 10 ml vial of the Regular Human insulin Novo Nordisk sells as Novolin costs about $20 at Wal-Mart. A vial of Novolog, Novo Nordisk's analog insulin, costs somewhere around $94. With that kind of price differential--the analog being almost five times the cost of the Regular--which of its two meal-time insulins do you think Novo-Nordisk is promoting to doctors?

But if you think that Novolog is almost five times as expensive as Novolin because it is five times better, you're making a big mistake.

The main difference between the two insulins is the speed with which they act. R insulin takes about an hour to start working and has an observable effect for 5 hours, where the Novolog starts acting within 15 minutes and is pretty much done at 3 hours.

But while this means that you can inject the faster Novolog when you begin to eat rather than having to plan ahead, speed is not always a good thing when you are talking about insulin. That is because if the fast insulin gets to your blood stream faster than your food, you have the risk of going low. And if your food takes longer to digest than you expect, the fast insulin can be all done long before your food is and you'll go high. This is why a food like Pizza, which has a lot of carb but digests slowly because of its fat content, can end up producing very ugly blood sugars when you use a fast insulin--a dip at hour hour followed by a nasty rise at hour 3 or 4.

R insulin, in contrast, dribbles in more slowly over a longer period of time. This means that if your food's speed of digestion is unpredictable, there's coverage for a longer window of time. Not only that, but because the insulin dribbles in more slowly than the analogs, if you are going low, you have more warning and can correct more easily. If you end up not eating as much as you expected, you don't experience a sudden WHOMP of insulin hitting a blood stream devoid of carb and you have time to hit the Smarties or glucose tabs or whatever it is you use to correct.

This slower speed can be particularly important to you Type 2s who are striving for very tight control. This is because, unlike the Type 1s who cover meals with insulin, you may still have some residual beta cell function, which means that when you use a meal time insulin your own phase 2 may occasionally kick in and mop up some carbs--especially after you've used insulin for a while and given those overwhelmed beta cells a little "beta cell rest." This can produce unexpected lows, and may be one reason why doctors rarely suggest meal time insulin for a Type 2 until their blood sugars are terrible and much harder to control with insulin or anything else.

Making R work safely, for a Type 2, requires that you keep your carb intake modest. While I don't officially low carb while using insulin, my daily intake is only around 100 to 120 grams--25 to 40 per meal. That's because my basic ground rule is not to take so much insulin that if something went seriously wrong, I'd face a life-threatening hypo.

By "going wrong" I mean that after injecting and having a few bites of your food, you start to throw up and can't keep anything down. Or after you inject there's a sudden emergency that has you rushing to your car to rescue a family member. Or even, after injecting you get so caught up in what you are working on that you completely lose track of time and forget to eat. These kinds of things happen rarely, but they do happen--especially the forgetting to eat part, so I stick with a dose of insulin that if it does produce a low, produces a low my own body's counterregulatory system can compensate for perhaps with the help of some glucose. Type 2s who are not low carbing, unlike Type 1s, usually have a robust counterregulatory system that will dump carbs from stored glycogen into the blood stream if you get down to the low 60s or worse.

With this in mind, and since I subscribe to Dr. Bernstein's dictum that "small inputs make for small errors" and have resisted the impulse to increase my insulin dose to try to cover any more carbs than 40 grams, which for me takes about 4 units to cover it. This means Pad Thai with its 100 grams of carb per serving is still permanently off the menu. But 40 grams is enough to let me have a nice slice of artisanal bread, half a potato, or a scoop of ice cream. I can have Chinese food (avoiding the stuff encased in fried dough) and a very small serving of rice. For me moving to 40 grams compared to the 12 grams I ate when low carbing, opens up a huge world of food choices and makes food much less problematic, while keeping the insulin to 4 units or less has, so far, kept me from ever seeing truly dangerous lows when something goes wrong.

I always check my blood sugar 3 hours after using the R to make sure I'm not going to go low, and if I'm in the low 80s or 70s by then, I'll have a couple grams more carb--and I mean a few--maybe 5 or so.

Another reason I like R insulin is that though it is pretty much done working at 5 hours, it has a very small residual effect that lasts up to 8 hours. For me, this means that if I use it for my meals, I don't have to use a basal insulin, because there seems to be enough insulin left in my system to keep me low through the first part of the night, but it's gone by that 4 AM period which is when I was waking up in a cold sweat when I was taking Lantus because of the early morning hypo.

There's one last benefit that I've observed with R insulin. I don't know if this would be true for other people, but it certainly is for me. Unlike the analogs, R insulin does not make me hungry.

I suspect it is because it is slower in action and my body interprets swift changes in blood sugar (or perhaps in insulin levels) as hunger. Whatever it is, when I was using Novolog, I observed that though I was getting very good blood sugars after eating, especially in restaurant situations, I was always hungry 2-3 hours later. With R insulin, I never get the munchies. In fact, I've noticed that I have no desire to snack at night, which is unusual for me.

Another thing with R insulin, which I find useful, is that I can delay its action a bit by injecting into the top of my leg, rather than the belly fat. My current regimen is to inject 3 units into my belly when I wake up, when I'm most insulin resistant, and into the top of the leg for the other two meals. I eat 25 grams of carb for breakfast, an hour after injection (it takes that long until I can face food, anyway, so waiting isn't a problem). I inject 3 or 4 units into my leg 5 hours after the morning shot, and 3 units 5 hours after that. Lunch and dinner are generally 30-40 grams of carb but with this schedule, I'm finding I can pretty much eat my meals when I want to without seeing bad highs. With the R slowed down a bit more with the leg injections, this is the closest I've gotten to the way I was eating while taking Ultralente, the discontinued insulin, which worked so well for me.

I've been waking up in the 80s-low 90s doing this, and staying between 80 and 120 after meals except when I've eaten something ridiculous. Even then the worst reading I've seen has been 143 and that was after eating something ridiculous. I'm not feeling my blood sugar go up and down, which makes me feel lousy. I'm remembering why it is that I like R so much.

The only other drug I take right now is 1500 mg of Metformin ER in mid morning, mostly because it keeps me from gaining weight. If I stopped taking it, I'd have to use another 1 to 2 units of insulin per meal to cover that 30-40 grams, but I'd be more prone to gain weight, especially now that I'm off my estrogen replacement for good.

Stopping the estrogen has boosted my insulin requirement a bit. I have been using 4 units where I would have been using 2.5 units in the past and 3 units where I would have used 2. But while quitting estrogen has made me more insulin resistant, my insulin resistance still does not begin to rise to the level of a typical Type 2.

Once off the estrogen, my almost 59 year old body seems to have decided it wants more fat--which is what bodies do when they are trying desperately to store what estrogen they can, since estrogen is stored in fat. The Metformin helps, but the chances are that I'm going to have accept some weight gain. It's better than cancer, and after all the years I have been taking estrogen, cancer risk was starting to become an issue. I've been lucky enough to be able to be a "hot babe" into my late 50s. Time to count my blessings and move on! Especially since, according to the research Kolata's book cites, a bit more weight at my age appears to correlate with better health and longevity.

Note: Weirdly enough, R insulin is available in most states without a prescription. If you need needles, you will probably need a prescription for those, but if you are already using syringes and wish to try R, all you have to do is walk up to the pharmacist at Wal-Mart, say, "Can I please have a vial of Novolin R," and pay your $20.

I find this very odd, but that's how it is. The plus side to it is that you can replace a vial without going through a major song and dance if something happens to it.

Drug Approval: Diabetes is NOT Advanced Cancer

A friend of mine took a wonderful drug last year. It gave him at least 3 heart attacks and put him into intensive care for more than a month. Another friend took a terrible drug. It raised his risk of dying of a heart attack.

Why is one drug that guarantees a heart attack good, and the other that only raises the risk of one bad?

Because of what the drug was prescribed for. The first drug was wonderful because it was given to treat Stage IV melanoma a, cancer which usually kills the patient within six months of diagnosis. There is currently no other drug treatment that works for State 4 melanoma at all. My friend is still alive and in what looks like good health 18 months after treatment with the drug that gave him his heart attacks. Because of the damage the drug did to his body, he knows he is not likely to live to be 80, but he may live to be 50, and for someone who was given 6 months to live almost two years ago, that is good enough.

The second drug was terrible because it was given to treat the high blood sugars caused by Type 2 Diabetes. Type 2 Diabetes can be fatal, but a diabetes diagnosis is not a crisis. It usually takes anywhere from 10 to 30 years of exposure to elevated blood sugars before diabetes kills its victims. If the patient can their blood sugars down into the normal range, they can live as long as anyone else. And many people do.

Unlike the case with the cancer drug, there are safe existing drug treatments available to patients with diabetes that work well and do not have the cardiac risk presented by the terrible drug. There is even a well-documented non-drug treatment for Type 2 diabetes, cutting the carbohydrates way down and adding exercise, that for many people works even better than the terrible drug and has no side effects. The only reason to take a new drug for Type 2 Diabetes is if it is safer and more effective than existing treatments. Any drug that worsens health in any way is not a good drug for this disease, because there are drugs that improve it already available.

Patients can tolerate side effects, even dreadful side effects, if a new drug may save their lives in a situation where they are otherwise facing certain death. It makes sense for the drug regulators to hurry a drug into production if it looks like it may provide even a few extra months to someone who is has no other options.

But the criteria for approving a drug intended to save a life where there is no successful treatment should be very different from those used to approve a drug for a chronic but not immediately life-threatening condition. Especially since drugs for chronic conditions are meant to be taken every day, week after week, year after year, so that over time the potential for side effects becomes much, much higher.

HOW WE MUST CHANGE THE WAY DRUGS ARE APPROVED

There needs to be different criteria for approving a drug intended to treat a fatal condition for which there are no effective treatments than there are for approving a drug meant to treat a chronic survivable, condition like arthritis or diabetes which may last for decades.

If there IS an effective treatment for a chronic condition, the drug company must be forced to prove that a new drug is both more effective and as safe as the existing drug.

The current FDA drug approval process does not ask that drug companies prove their drug is better in controlling symptoms than drugs already on the market. It only requires that the drug perform better than a sugar pill. It does not ask drug companies to show that their drug is safer than existing, effective treatments.

As a result, we are seeing new treatments brought to market, like Avandia, Vioxx, and Januvia that are not any more effective than existing treatments, but which have much higher risk profiles--or, as in the case of Januvia, risk profiles that are unknown because no research has been done to identify the subtle, but possibly serious, long-term side effects caused by inhibiting the action of an enzyme used throughout the body.

ENHANCED FOLLOW UP TRACKING SHOULD BE REQUIRED

Once a new drug is approved for a condition where an existing, effective drug exists, it should be prescribed only after patients have tried the known, proven drugs for this condition.

The FDA should institute rigorous follow up tracking of the drug. Each new patient put on a drug should be required to file a report after three months of taking the drug listing any side effects they have experienced with the drug. Doctors should be required by law to perform any test that the drug prescribing information suggests.

The current aftermarket tracking system current system makes it so time consuming to report a side effect that doctors rarely do it, and few patients even know that they can report a side effect. That is why it takes five or more years for serious side effects to surface, though thousands of patients have been experiencing them all along.

After the drug has been on the market for a year, the FDA should require investigation of any side effect that is reported by a significant number of patients. The side effect tracking should continue until the drug is five years old.

By forcing patients to report side effects of brand new drugs, the FDA would be giving patients the message, "This drug is new, its effects are unknown, and yes, you are a guinea pig." If patients know this and are willing to take the risk the new drug represents, fine. But they won't be, as is the case now, taking new drugs in the naive belief that their dangers are already understood.

PREVENT UNSUPPORTED CLAIMS

Finally, drug companies must be prevented from promoting new drugs by claiming they do things that are not proven by high qualify research that has been carefully examined. The makers of Avandia and Actos should have been prohibited, by law, from claiming that their drugs rejuvenated beta cells. The makers of Byetta and Januvia should face the same prohibition, until that effect has been conclusively proven by research.

Most of the most dangerous drugs have been promoted by well-financed drug company campaigns that told doctors that their drugs did highly desirable things they turned out not to do. Doctors, alas, do not have time to investigate the research on which such claims are made. If drug companies were prevented from marketing their drugs to doctors with these inflated claims, doctors would be a lot less likely to prescribe new drugs until they were better understood.

Researcher threatened with $4B Suit for Avandia Warning

Here, from the Boston Globe, are more details about how John Buse, the mainstream researcher who will be the next ADA presidents, was threatened by GlaxoSmithKline, the maker of Avandia, for calling attention to its tendency to cause heart problems.

Scientist says executive of Avandia firm tried to bully - Boston Globe

From the article:

"An executive of the company that makes the diabetes drug Avandia said a researcher who was among the first to link it to heart problems would be held liable for the $4 billion GlaxoSmithKline PLC lost in stock value as a result of his findings, Dr. John B. Buse testified before congressional investigators yesterday.

This information came from testimony, under oath, to congress.

"Buse told the House Committee on Oversight and Government Reform that he raised concerns about Avandia's connection to heart problems in 1999 , the year the Food and Drug Administration approved it for sale. He said the Glaxo executive, Dr. Tadataka Yamada, made the "disturbing" comment during a meeting Yamada had with Buse's department chair at the University of North Carolina." [emphasis mine]

Those of you who keep defending the drug companies really need to think about this. This happened eight year ago--EIGHT YEAR AGO! Not a word of this kind of tactic leaked to the press until now, probably because Buse and his bosses knew that the drug companies were capable of instituting a lawsuit like this which, win or lose, would cost them and their university many millions of dollars they couldn't afford, though it would be lunch money to Glaxo.

So the threat worked.

You have to ask yourself: How many other researchers who have found other problems with high-profit drugs have been the victims of this kind of threat? What other problems have been hidden because drug companies threatened researchers or their institutions this way?

We may never know, because this kind of threat can be very effective. So can the threats to stop funding research at a researcher's university or medical school if he or she doesn't shut up.

It is starting to look like the morals and operating strategy of the big legal drug pushers isn't a whole lot different from that of their bush league compatriots selling the illegal stuff. When a drug earns you 3 billion bucks a year, who cares if some people are dying unnecessary deaths. If someone looks like they're going to mess up those juicy sales, well, you knock them off. Machine guns are unnecessary. Just threaten them in a way that shuts them up. In this case, it looks like the threat worked very well.

The article also points out that " Glaxo waited 11 months before telling federal regulators about clinical trial results linking Avandia to heart risks." That is 11 months during which someone's mom, grandma, dad, or husband developed heart failure that would kill them.

Final thought: With Buse in line to head the Drug Company and Junk Food Conglomerate-owned ADA, will he knuckle under to their threats to cut ADA funding if he suggests that, just maybe, carbs are NOT the other white meat?

Avandia/Actos Problems Well Known in 2003

I just did a search of the alt.support.diabetes newsgroup to see when, exactly, I became aware of the significant problems with Avandia and Actos that just made the medical news this month.

It was in 2003.

Here are the side effects I posted about along with the date of the posting and the thread title in case you want to look up the old messages yourself. All postings were made under the username "Jenny." The posted text is in italics.

1. Heart Failure:

Posted on a.s.d. on Oct 24, 2003. Thread name: Metformin & Glyburide should I change meds?:

Actos and Avandia (a similar drug) have their own problems--notably a tendency to cause weight gain and worsen heart failure. Also, they have not been on the market long enough for us to really know what their long term effects might be. They are related to Rezulin which was pulled off the market after an initial success for causing a number of after-market deaths through liver failure

On Jan 18, 2004 in the thread "Problems with Actos":


Thiazolidinediones Contraindicated in Patients at Risk for Heart Failure
CME [Medscape]

News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD
Release Date: December 8, 2003; Valid for credit through December 8, 2004
Dec. 8, 2003 - A joint statement from the American Heart Association (AHA) and the American Diabetes Association (ADA), published in the Dec. 9 issue of Circulation, urges physicians not to prescribe thiazolidinediones (TZDs) to patients at risk for congestive heart failure (CHF). The statement will also be published in the January 2004 issue of Diabetes Care.

The message goes on to reproduce the entire text of the CME including the warning that patients who gain more than 6.6 lbs should be watched very carefully.

The text of the article reporting the macular edema was repeated in this thread too.

2. Liver Failure.

Posted Oct 24, 2003.Thread name: Metformin & Glyburide should I change meds?:

Coincidentally, I just read an article today online on the American Academy of Family Physicians site http://www.aafp.org/afp/20010501/1747.html that said that:

"Although results from pre-marketing trials revealed no evidence of hepatotoxicity with the newer agents (rosiglitazone and pioglitazone), two recent case reports demonstrated that rosiglitazone [AVANDIA] may be associated with hepatic failure following just 14 days of therapy, although a true cause-and-effect relationship has not been established.""

3. Macular Edema.

Posted Nov. 19, 2003. Thread name: Avandia/Actos associated with Macular Edema:

From Medscape:
http://www.medscape.com/viewarticle/464732
November 19, 2003

Glitazone Use May Be Associated With Macular Edema in Diabetics

Karla Harby

Nov. 19, 2003 (Anaheim) - Results of a retrospective chart view suggest that glitazone use may be linked to the existence of macular edema in patients with diabetes, according to a study presented here at the annual meeting of The American Academy of Ophthalmology.
[Entire article follows]
=================

If this information was public enough in 2003 that a humble reader of newsgroups and Medscape knew about these significant side effects, why didn't doctors? The current medical press coverage makes it clear that doctors have been prescribing these drugs to people who were at known risk for heart failure.

Considering how many people have posted on the newsgroups over the years about how they experienced sudden, very intense weight gain and swelling while taking these drugs, and that they have also posted that their doctors told them to keep taking them in the hope the drug would rejuvenate beta cells, it isn't a surprise that there are "excess" deaths attributed to these drugs.

The really scary thing to me as this story unfolds is the way in which reputable medical organizations are still urging people to keep taking these drugs despite the growing evidence that they may be very harmful--and without even mentioning their contribution to Macular Edema or Osteoporosis.

A few people have emailed me that my "attitude" towards new drugs and their side effects would keep any drug from being approved, but that isn't the case at all. What my "attitude" would do is ensure that the drug approval process would:

1. Insist that drug companies be required to document in detail HOW their drug works, not, just as is the case now, that the drug works, though the cause may be mysterious or, as in the case of Avandia, attributed to causes that turn out not to be true like beta cell regeneration or redistribution of fat from the abdomen to thigh.

2. Insist that drug companies investigate more thoroughly other physiological effects of a new drug, especially those related to its mechanism.

That way approval of a drug like Januvia, that inhibits a specific enzyme would require that researchers investigate how the drug affects the OTHER known functions of the enzyme being affected and ensure that inhibiting the enzymes does not have a disastrous effect on some system besides the one the drug is being used to effect. As it is now, though we know DPP-4 plays a huge role in immune system regulation, there have been no studies to see why it is raising leucocyte counts in people taking Januvia or whether it might promote melanoma, a cancer known to be suppressed by DPP-4.

In the case of Avandia, the drug companies knew pretty early that it was growing new fat cells, but did not look at the process and learn that the new cells were being made out of bone precursor cells. They also knew of the edema but did not investigate the effects of this edema on the heart function of people who had not yet been diagnosed with heart failure. It is very possible that the large water burden these drugs add to the body cause subclinical heart failure.

Yes, this additional testing would be expensive--though nowhere near as expensive as the hundreds of millions of dollars spent on TV and press campaigns intended to get you to buy the drug or the many millions spent on enticing doctors to prescribe it. But if you or a loved one are one of the people who is going to die because of a poorly understood "side effect" of a new drug I bet you'd want that research money to be spent.

ONE LAST NOTE: AN INTERESTING POLL

http://diabetes.about.com/b/a/000114.htm

This poll taken by About.com's diabetes editor shows that 50% of those reporting that they took Avandia experienced side effects. The most common was edema, but 5% reported developing heart failure and 4% reported worsening previously diagnosed heart disease.

These numbers reflect the kinds of anecdotal reports we've long been hearing in online bulletin boards.

Kolata's "Inconvenient Truth" for Dieters

New York Times science reporter Gina Kolata has hit a home run with her new book, Rethinking Thin: the New Science of Weight Loss--and the Myths and Realities of Dieting. If you've ever tried to lose 20 lbs and failed, or if you think you are doomed because you can't lose the weight your doctor tells you you have to lose, you really need to read this book.

What Kolata has done in Rethinking Thin is to summarize the findings of mainstream research into the causes and treatments for obesity. What she finds is that, as is so often the case, well-conducted research that flies in the face of what people think ought to be true gets ignored, even when it has very important messages to communicate. Even people who consider themselves scientists are unable to accept results that tell them things they don't want to hear.

Among those things--supported by solid research done by scientists at top research organizations are these:

1. Fat people who achieve normal weight have bodies that behave like those of people undergoing severe starvation which results in changes in the brain that force the body to obsess about food and do whatever it can to regain the lost weight.

2. Because of the physiological changes caused by losing a large amount of weight, a once obese person who has achieved a normal weight has developed such a hyper-efficient metabolism that they really do gain significant weight eating 1/2 the calories that an always thin person of the same weight and build eats. This has been verified in experiments where people are kept virtually imprisoned and every morsel they eat is weighed and measured, along with a dizzying list of metabolic products they give off.

3. Every large scale diet study over the past generation no matter what diet it tested found that few people are able to maintain even a 10% weight loss over a year.

4. Children adopted at birth have body compositions at adulthood that match very closely to those of their birth parents, no matter what they ate or saw modeled by the parents in their adoptive homes. This is very strong evidence that weight is determined by genetics.

5. Several massive intervention experiments with school children who were carefully educated about diet and exercise and fed "healthy "foods found that the children learned the information but it made NO difference in their weight.

and finally, and most importantly:

6. Research data with impeccable statistics shows that people who are overweight (though not obese) are less likely to die than people who are very thin or very fat.

7. Some well-respected obesity researchers believe it is possible that the fattening of our population is a byproduct of the fact that we are raising our children from pregnancy on in a far safer, better fed environment than has ever before been seen, and that this is resulting in early remodelling of the systems of the brain that control food intake in a way that promotes weight gain.

Most interestingly, the studies you are always hearing cited in the handwringing articles the media loves to feature about the "obesity epidemic," --those studies that supposedly showed higher mortality among the overweight--cherry picked their participants to get the result they were looking for. At times they screened out as many as 90% of the people in the study to find those who would support the expected results.

These studies also relied on the participants' report of their weights rather than actually weighing them despite the fact that researchers know people almost always report lower weights than they really have. The data from the large scale NHANES study that periodically samples the U.S. population, where the participants were actually weighed, and where they were drawn from society as a whole, not carefully chosen sub-groups, found that overweight correlated with better health.

WHAT DOES THIS MEAN FOR PEOPLE WITH DIABETES?

It means what I've been hammering away at for years: when we talk about "Diet" for diabetes, we should NOT be talking about achieving some impossibly low weight that has eluded most of us for years despite heroic attempts to achieve it. "DIET" for people with diabetes should mean "Eating foods that don't raise our blood sugar."

If you eat in such a way as to keep your blood sugar normal, you'll have the same health as any other person of your build, which if it is overweight (rather than obese) means you may be healthier than the super-thin supermodels you've been longing to be.

That said, the one thing I wish had been mentioned in the book, which wasn't, is the possibility that the genetic changes that cause obesity may also be a result of the rising concentrations of pesticides and industrial chemicals in our water and air and all the foods we eat.

Because experiment after experiment has shown that people without certain genetic traits cannot become fat even when fed 3 times as much as they normally eat, it is probably safe to say that people who are obese DO have some genetic damage going on. The fact that good research also shows that obesity is more frequent among the poor--who live in environments more likely to be polluted, contributes to this suspicion.

How Glaxo Tried to Silence Concerns about Avandia: NYTimes

Today's New York Times reports that John B. Buse will testify to Congress about the attempts made by Glaxo, the company that sells Avandia, to silence his criticism of the drug. Buse is keeping the details close to his chest before his testimony, but reading between the lines in the article, it looks like Glaxo, a huge contributor of research funds to his university, may have threatened they'd cut those funds if he didn't shut up.

Buse will be the next head of the ADA, which makes it pretty sure he isn't a rogue, rabble-rousing extremist. So whatever Glaxo did to inspire him to bite the hand that paid for his research must have been pretty bad.

Doctor Says Drug Maker Tried to Quash His Criticism of Avandia
http://www.nytimes.com/2007/06/02/business/02drug.html

Note that Dr. Buse was already expressing his concern about Avandia in 2000, seven years ago. Even more troubling is this information taken from the same article. "The following year [2001], after demanding that Glaxo strengthen the language on Avandia’s label describing its potential heart risks, the F.D.A. sent Glaxo a letter reprimanding the company for playing down those risks in discussions between sales representatives and undercover investigators at a medical conference."

That was 6 years ago. The company was given a meaningless slap on the wrist, went on to sell 7 million more prescriptions of the drug worth many billions of dollars, and the FDA ignored the evidence its own investigators found that Glaxo was lying to doctors about a drug that they already knew was causing unnecessary heart deaths.

The issue goes way beyond Avandia. Every drug you are taking that is still under patent may be the subject of the same kind of strong arm tactics and fraud that you see revealed here. If it took 7 years and untold numbers of unnecessary deaths (I've seen numbers like 10,000 and 20,000 bandied about in the medical press) to get anyone to go to the media about the safety of Avandia, you can be sure that there are other equally dangerous drugs being promoted heavily to your doctor.

More importantly, since your doctor, like most, probably gets his or her information about drug safety from the drug companies who sell the drugs, and since these companies do lie about safety issues, you cannot trust your doctor's assurance that a drug is safe.

So what can you do?

1. Before you take ANY new drug, download the "Prescribing Information" for that drug. This is a legal document. It has to be kept up-to-date. It is the "label" you see mentioned in articles about the drug. Unfortunately, years ago the drug companies got the FDA to remove the requirement that a copy of this information be given to consumers when they purchased the drug at a pharmacy, and many people do not even know this important document exists.

The Prescribing Information will list all the known serious side effects of a drug. When the FDA issues a slap on the wrist, it makes the drug company mention the side effect in the Prescribing Information. The Avandia Prescribing information has listed heart failure as a concern for years and last year it added macular edema (swelling in the retinal area that can cause blindness.)

2. Make sure you understand the Prescribing Information. If your medical knowledge isn't good enough to understand the wording, do not be shy about calling up your doctor and asking him to interpret it to you. The information may be as big a surprise to your doctor as it is to you. When I have asked doctors about information in the Prescribing Information, including black box warnings, they have often not known it was there.

3. If there are serious side effects, ask your doctor whether there is testing that can spot these side effects early enough to prevent permanent damage and make sure your doctor does those tests. Even here, there is the concern that the drug company may have told your doctor that certain tests can guarantee safety when this is not true.

For example, with some drugs, including Rezulin, by the time your liver function tests came in abnormal, the damage was already done and you might not recover. With Zyprexa, by the time your blood sugar is abnormal, you may have sustained irreversible damage, too. Since we learned that the drug companies selling these dangerous drugs may offer insurance to your doctor to cover claims if you sue him after experiencing kind of permanent damage as an incentive to get him to keep prescribing a dangerous drug, as was done with both Vioxx and Zyprexa, you can't trust your doctor's assurances 100%.

4. Ask if there is an older, better understood drug or other healing strategy (like exercise and diet) that could be used instead of the newer drug. In the case of Avandia, diet and exercise provided much better outcomes for people with diabetes and prediabetes than did the drug. The alternative drugs or strategies are usually much cheaper, too.

5. If a doctor makes a claim that a new drug does something really important no other drug does and that is why you should take it, investigate the data on which that claim rests.

Many people with diabetes were told that Avandia would rejuvenate their beta cells, and that was why they should take it even if they were gaining tens of pounds and swelling up like ticks. This turns out to have been a claim based on the most flimsy of evidence--much of it derived from the study of another, more dangerous drug no longer on the market--that was recently completely disproved by the DREAM study.

Vioxx was sold with the promise that it didn't cause the stomach bleeding other NSAIDS cause, which was also false. (My mom ended up in the ER thanks to stomach bleeding from Vioxx.) More recent data shows that Vioxx and related expensive, dangerous, new drugs are no more effective than Ibuprofen.

Right now, people taking incretin drugs like Byetta are being told that this drug will rejuvenate their beta cells, but the evidence for this is also weak and is derived from mouse studies. One fact everyone with diabetes must memorize is this: Rodents have very different pancreas function from humans and many drugs have effects on rodents that they do not show in humans.

All this sounds like a lot of work, and it is. But since your doctor is too busy to do it, you will have to. It is YOUR body that will pay the price if you take a toxic drug.