Friday, June 29, 2007

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

Wednesday, June 27, 2007

$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?

Tuesday, June 26, 2007

Study REALLY Proves Byetta Sucks for Most Type 2s

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.

Monday, June 25, 2007

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.

Saturday, June 23, 2007

Januvia and Melanoma

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.

Wednesday, June 20, 2007

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!

Monday, June 18, 2007

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


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!