September 26, 2010

Surgical Site Infections Rise Dramatically when Blood Sugar is over 140 mg/dl

Though doctors call them "diabetic" complications, many studies conducted in cell cultures, animals, and humans, which you can read HERE, point to the conclusion that organ damage due to high blood sugars starts at levels that doctors label "prediabetic."

Now another study--one that looked at the factors causing post-operative infections has come up with the same finding.

The study is:

Postoperative Hyperglycemia and Surgical Site Infection in General Surgery Patients Ashar Ata et al. Arch Surg. 2010;145(9):858-864. doi:10.1001/archsurg.2010.179

You can read a good summary of this study, with more information than is found in the abstract here: Science Daily: Postoperative High Blood Sugar Appears to Be Associated With Surgical Site Infection

The researchers examined the records of 2090 patients. For 1561 of these patients, blood sugar measurments were recorded and 803 of these blood sugar measurements were taken within 12 hours of surgery.

The researchers found that in the group as a whole the following factors were predictive of surgical site infection (SSI):
increasing age, emergency status, American Society of Anesthesiologists physical status classes P3 to P5, operative time, more than 2 U of red blood cells transfused, preoperative glucose level higher than 180 mg/dL... diabetes mellitus, and postoperative hyperglycemia.
But here's where things get interesting. Because the researches found that,
After adjustment for postoperative glucose level, all these variables ceased to be significant predictors of SSI; only incremental postoperative glucose level remained significant.
And what was the postoperative glucose level at which bad things started to happen?

Readers of this blog, don't all answer at once, but you're right!

It was 140 mg/dl the very same blood sugar level we have long been telling people with diabetes should be the very highest they ever let their blood sugar reach if they can possibly avoid it.

In the type of surgery studied in which post operative infection was by far the most common--colorectal surgery, where 14.11% of patients suffered infections, the researchers found that those with blood sugars higher than 140 mg/dl were over three times more likely to suffer infection as those without.

Science Daily also quotes the full text article as saying,
In conclusion, we found postoperative hyperglycemia to be the most important risk factor for surgical site infection in general and colorectal cancer surgery patients, and serum glucose levels higher than 110 milligrams per deciliter were associated with increasingly higher rates of post-surgical infection.

What makes this study so important is this: If you go in for a major procedure it is almost 100% certain that, despite your protests, the anesthetist will hook you up to a glucose drip before surgery. This guarantees that no matter how perfectly you have been eating, your blood sugar will be at least 140 during your surgery--a number that surgeons, trained to believe that 200 mg/dl (11.1 mmol/L) is "Diabetic" will tell you was a "nice normal blood sugar" as mine did.

The only way to avoid this is to negotiate it with the surgeon before you commit to the surgery and get it in writing in a form that you can give to the hospital staff before the surgery.

No matter what you have been told orally, the staff in the hospital will listen only to the surgeon and pay attention to you only if they see written instructions that look like they could lead to a law suit.

Unfortunately, if my experience is anything to go by, getting such written instructions may be impossible, even with an otherwise excellent surgeon. Therefore, it would be a good idea to print out this study and keep it in your file of important medical papers so that you can take it with you when you have your preliminary meeting with the surgeon.

Once your surgery is done, you are not out of the woods. The food you will be given in the hospital will be the "diabetic menu." This may be called a "Carb-controlled diet" (It was at the hospital I stayed in) but this is misleading. It is, in fact, the same old dangerously high carb/ low fat diet that nutritionists still defend to the death--the death of the patients with diabetes who eat it.

For breakfast you'll be offered toast with jelly but no butter, cereal with skim milk, and sugary fruit, so that you face the choice of starving or raising your blood sugar well over that 140 mg/dl level. The rest of your meals will be thin slices of fat free mystery meat and starchy veg, with fruit--canned in corn syrup--for dessert.

Again your only defense here is signed orders from your doctor, which may be very hard to attain. That is because most doctors do NOT understand that the carbs you eat are what raise your blood sugar. They really don't.

And they remain convinced that blood sugars up to 200 mg/dl are not dangerous and that it is a mysterious disease called "diabetes" that harms people, not exposure to high blood sugars.

Doctors also believe, without question, that high fat diets cause heart attacks and that it is much healthier for you to eat that toast and jelly than a fresh egg.

So before you go into a hospital for elective surgery, if possible, get a letter, signed by your surgeon or another doctor who practices at the hospital where you are having your surgery ordering the nutrition staff to allow you to order at will from the regular menu and forbidding them to make you eat foods from the "diabetic" menu.

If it isn't possible, arrange for friends or family members to bring you the foods you need to eat to keep your blood sugars normal. Arrange to go home where you have control over your food supply as soon as it is possible.

If you are forced to go to a nursing home after surgery, make sure that your doctor orders the nursing home staff to allow you or a chosen family member who understands your dietary needs to control what you eat and, again, forbid the use of the "diabetic" diet. Otherwise, you will be forced to eat the high carb/low fat diet that will raise your blood sugar and make surgical infection more likely.


September 24, 2010

Avandia Finally Gone but Actos is Just as Dangerous

The FDA has for all practical purposes killed Avandia. Patients will have to be given a scary disclosure form to sign if it is prescribed and it can't be prescribed without the doctor filling in paperwork explaining why the patient couldn't be put on Actos.

The flaw here is that Actos is just as dangerous a drug. Here is a brief list of the problems with Actos. You can find the citations to the studies backing up each of these statements on this page: Actos and Avandia: Dangerous Diabetes Drugs.

1. Actos can cause heart failure in young people who did not have any signs of heart failure before taking it. Heart failure is a weakening of the heart muscle that is almost always fatal after a number of years of increasing debility.

2. Actos taken over long periods of time damages the structure of the arm and leg bones in a way that causes fractures. By the time these fractures occur, it is too late to do anything about the damaged bones because how Actos works is that it turns the stem cells that should have turned into bone cells into fat cells which absorb glucose and turn it into body fat. That's a heckuva way to lower blood sugar, but that is what it does.

3. Actos makes people gain weight in the form of new fat cells that they are stuck with forever even if they stop the drug. (See #2 for why.)

4. Actos has been shown in studies to be less effective than the wimpiest high carb dietary changes (mostly calorie restriction) and mild exercise. Actos is far less effective than the adoption of a diet of 100 g a day of carbohydrate or less.

5. Actos causes macular edema--i.e. swelling in the most sensitive part of the retina which causes blindness.

6. Actos appears to raise the risk of bladder cancer. This occurs when the drug is taken for a longer period or at higher doses.

You risk all this in exchange for an average drop in A1c of .2% (at the 15 and 30mg doses) and .9% drop at the 45 mg dose at which bladder cancer becomes an issue. And those drops are in a population whose average A1c was 10% at the start of the study, meaning that after taking this dangerous drug for 6 months they still had A1cs in the 9% range we know will cause blindness, amputation, kidney failure and heart attack death. That finding is reported, somewhat deceptively here:

Official FDA Required Actos Prescribing Information

In contrast to this miserably poor improvement, hundreds of people who cut down on their carbs following the advice you will find HERE report dropping A1cs from 10% or more down to the 5%-6% range at which complications are very, very rare.


September 18, 2010

Why The New Drugs Cause Such Terrible Side Effects

Yet another piece of bad news showed up--without mainstream coverage--in the health news this week. A long term study of Actos discovered that there is a clear dose and time-related increase in bladder cancer among those who take it.

As MedPage Today reports:
An interim analysis of data from the study, which includes more than 193,000 patients with type 2 diabetes, revealed no statistically significant increase in bladder cancer among pioglitazone users compared with nonusers (hazard ratio 1.2, 95% CI 0.9 to 1.5), but "the risk of bladder cancer increased with increasing dose and duration of [pioglitazone] use, reaching statistical significance after 24 months of exposure.
Of concern to all of us should be the way that the company that makes the drug attempts to wave off this latest of many findings that show how their drug ruins lives. Takeda's spokesweasel claims, "the data did not reach statistical significance for the primary endpoint of increased risk of bladder cancer."

What this means is that even though the data shows a very strong relationship between bladder cancer and their drug when a larger dose is taken for 2 years, the relationship disappears when you add into your statistical pool all the people who took it for a shorter time period or at low doses.

If you can't see the problem with this argument, I worry about you.

Apparently the renegade doctors who earn huge salaries hyping drug company products have decided a drug is only dangerous if it kills large numbers of those who take it, not just a measurable number of those who take it at commonly prescribed dosage levels for several years.

But that's not what I'm blogging about here. What I'm blogging about is why so many of the new drugs have such terrible side effects and why we only learn about them ten to fifteen years after the drug is on the market.

The reason is this. Today's newer generation of drugs target specific genes and cell receptors. The TZD drugs, Actos and Avandia, target the PPAR-gamma transcription factor which regulates genes that affect how lipids are stored. No one questions that they do this, or that in a significant number of patients (but by no means all who take them) they lower blood sugar.

The problem is that PPAR-gamma regulates genes involved in a bunch of other processes in the body, too--processes that have nothing to do with blood sugar control.

PPAR-gamma, for example, transforms the bone stem cells that should turn into new bone into new fat cells. This is why after a decade on the drug many people start experiencing broken bones in their arms and legs (the areas where PPAR-gamma is most active) and why once bones begin to break there is no cure. A decade of rebuilding has been subverted and the weakened structure of the bone cannot be fixed.

And this points to the huge problem with the drug regulation process. There is no requirement--none, zilch--that a company applying for permission to market a new drug investigate what OTHER physiological processes are affected by the drugs's mechanism. All the drug company has to show is that it achieves what they are selling it to do. In the case of Actos and Avandia, that means causing a very modest drop in A1c--about .5%.

If course, if a drug undergoing the approval process does something that is severely damaging right away, the problem will show up during the approval testing. If lots of people's skin peels off, or lots of people have strokes, a drug won't usually get approved.

But most of the unintended consequences of the way new drugs work are more subtle and don't cause dramatic events during the first year or two that a person takes them. Many of these life-ruining side effects happen so slowly they don't show up for five to ten years--and then it takes a lot of work to link the side effect to the drug.

Many of these side effects are never linked. Doctors expect to see people with cancer in their practices and don't connect the cancers with a drug the person has taken for a decade. They expect to see heart attacks in people with diabetes and don't know that more people are having heart attacks than expected and that this is because of some drug they prescribed four years before.

It is only when the side effect is odd that anyone notices at all. If young people with no sign of heart disease suddenly develop heart failure as happens with both Avandia and Actos, a few doctors notice and report this to the FDA. (Many of course, don't.)

If people start breaking arms and legs--an odd pattern for osteoporosis--as happens with both Avandia and Actos, a few more doctors notice.

But the fact that a few doctors notice and report doesn't mean that other doctors hear about these side effects since they get all their "drug education" from drug company sales reps, those pretty young ladies who used to be college cheerleaders who show up at the office bringing such welcome take out lunches.

And the FDA will not pull a drug from the market when evidence of these more subtle side effects emerges either. It takes years to kill a dangerous drug--years during which the company that sells it continues to rake in its billions.

Cancer is a particularly troubling side effect of newer drugs, because the public believes, erroneously, that the drug approval process keeps cancer producing drugs off the market.

This turns out not to be true. Though drug testing eliminates drugs that cause cells to become cancerous in a test tube over a few weeks or which cause malignancies over the short life spans of rodents, it cannot identify drugs that change how the body fights cancers in ways that allow slow developing human cancers to gain traction.

That is why evidence a that a drug is raising the incidence of cancer rarely appears until a drug is almost at the end of its 14 year patent period. It has taken more than 12 years to notice the link between bladder cancer and Actos. It took nine years after its approval for anyone to notice the signal suggesting that Diovan raises cancer incidence by about 8%.

And that's why it won't be until another nine years or more that the public will learn that any drug that inhibits DPP-4 is turning off an immune system mechanism essential to fighting melanoma, prostate cancer, ovarian cancer and lung cancer. Details HERE.)

Even when the link between a drug and a serious, even fatal, side effect finally made clear by large population studies don't expect the drug to be taken off the market. There will be panels and hearings and FDA deliberations, but if the history of Avandia is anything to go by, the drug will still be selling at your local pharmacy five years after its clear what its real dangers are.

Because these secondary effects don't kill everyone who takes the drug, or 50% of them or even 10%, the drug company spokesweasels will argue, as the Takeda one does above that unless it is damaging everyone who takes it, it's still a good drug. They will also claim--though there is not a scintilla of evidence to support this claim, that the drug is saving many other lives which balance out the ones we know it is taking.

The only oral diabetes drug for which there is conclusive evidence that that it prevents deaths is Metformin, which has been on the market (in Europe) since the 1950s.

And not so incidentally, Metformin is the only oral diabetes drug that has not been linked conclusively with causing a fatal side effect. Though it was long thought that it might, rarely, cause lactic acidosis, that has been disproved. We now now that the incidence of lactic acidosis in those taking metformin is identical to its incidence among those not taking it.

But there is no evidence that the expensive newer diabetes drugs do anything but lower blood sugar very slightly--much less than dietary changes and exercise can do. There is no evidence any of these newer drugs are saving lives. And because when the drug companies go looking for this evidence, they keep finding the opposite--it was that kind of study that stopped the profits rolling in from Avandia--don't expect to see such studies funded in the future.

Is there any way to detect these life-ruining side effects before several million people have taken the drug?

A very good place to start would be to require that drug companies investigate the effect of a new drug on all the known expressions of the gene, transcription factor, protease or other physiological component it is known to impact. This information is widely available. There are databases online that link to all the research about every gene for example. A reasonable person should be able to read through these studies and determine which impacts might cause harm. Then those effects could be investigated as part of the approval process.

Doing this would have given us the answer we need about whether inhibiting DPP-4, a protease known to fight cancers, raises the incidence of the DPP-4 sensitive cancers--research that researchers say should be done, but that has not been done.

Drug companies will tell you this is too expensive and that such regulations would mean no more wonder drugs.

But when wonder drugs are clearly killing tens of thousands of people who would otherwise have lived, you have to ask yourself how wonderful they really are. We went to war over an attack that killed less than 3,000 people. But we let drug companies sell products that may be killing tens of thousands unnecessarily. Even though there is good evidence that the drug companies know their products are causing unnecessary deaths and hiding this evidence so they can continue to rake in their billions.

Isn't it time this changed?

September 13, 2010

Diabetes Drug Interactions Can Harm You

One of the most disturbing things about now doctors practice medicine today is that they very often don't know about the way that the different drugs they prescribe interact with each other, and some of these interactions can be quite dangerous.

I learned this the hard way over the past few months.

I had long known that Dr. Andrew Hattersley, who is the world expert on the form of MODY diabetes I appear to have, believes that long term people with MODY do better on insulin stimulating drugs like Sulfonylureas.

For years I ignored this, as the tiniest dose of a Sulf drug caused me to hypo dramatically. Then I ran into some new data which suggested why this might be true: it turns out that a substance, C-peptide, which is a by-product of insulin secretion, by the beta cell may play a protective function for nerves. When we inject insulin, we don't get that C-peptide.

So last winter, after years of doing very well on low dose fast acting insulin at meal time, I decided to switch to the one, much milder, insulin stimulating drug that I'd learned in the past I could take without hypoing, Prandin.

Prandin is marketed with the information that it is very short acting--and is out of the body in about 3 hours. I had tried it a few years ago and this seemed to be the case.

What I didn't know--and learned the very hard way--is that this is only true if you take Prandin alone--without Metformin. If you combine the two, it turns out that the Metformin blocks the mechanism in the liver that eliminates Prandin and the drug ends up being much, much more potent.

Very oddly, this interaction is not listed in the "drug interaction" section of the Prandin Prescribing Information insert. You learn it only by paying attention to a chart displayed in the clinical trial section of the Prescribing Information.

It is there that we learn that, over a 4-5 month period, people taking Prandin alone saw their blood fasting blood sugar rise by an of 8 mg/dl, and people taking Metformin alone saw an average drop in their fasting blood sugar of 4.5 mg/dl, but people taking both drugs simultaneously experienced an average decline in fasting blood sugar of 39.2 mg/dl--almost ten times as much as with Metformin alone!

A1c dropped dramatically in the combination group compared to the groups taking each drug alone, too.

Since the combination of the two drugs was giving me extremely normal blood sugars (fasting in the 80s rather than the high 90s I get with insulin and post meal numbers never higher than 140 mg/dl ) I was happy. I loved not having to fuss with injections or having to worry about my insulin losing its potency in heat or cold.

Until recently, when after taking Prandin for about 8 months I started to experience severe hypos. How severe? In the very low 40 mg/dl range. And the only tipoff I had that something was going on was seeing some oddities in my visual field. No shakes, no pounding heartbeat. In short, no hypo awareness.

To make it worse these hypos turned out to be resistant to glucose. After seeing a 43 mg/dl reading on my meter I immediately downed 15 grams of glucose which should have raised my blood sugar to the 110s but when I tested 15 minutes later my blood sugars were still in the 40s. At that I glugged down a can of sugary soda and after that my blood sugars finally rose to the low 90s.

What made these hypos all the more confusing is that in the past when I was injecting insulin I could not get my blood sugar to drop any lower than the mid-60s no matter what. Any time my blood sugar went lower than the low 80s I'd get a fierce counterregulatory response that would give me shakes, a high pulse, and all the classic hypo (or false hypo) symptoms. Suddenly my hypo awareness was gone.

I'm not entirely sure what changed--these hypos happened a full eight months after I started using the Prandin/Metformin combination and I had not been seeing hypos before that. It is possible I was having milder hypos but not catching them because of the lack of symptoms, but who knows?

It is also possible that another drug I was prescribed--the blood pressure medication hydrocholorothiazide (HCTZ), a diuretic, played a part in the loss of hypo awareness.

Any drug that causes my beta cells to secrete insulin on their own at meal times seems to cause my body to hold on to salt and that, in turn, raises my blood pressure. Only HCTZ which flushes out extra salt lowered it. So I was taking one low dose HCTZ pill every 3 days which was keeping my blood pressure stable.

A Google Search came up with one site that wrote, without attribution, that HCTZ affects the autonomic nervous system which I know is involved in the counterregulatory response. So it is possible that the HCTZ was what turned off the hypo awareness. And indeed, it looked as if my hypos were happening on the day when I took my HCTZ.

But outside of that one line posted somewhere on the Internet I could find no other warning that HCTZ could turn off hypo awareness. In fact, everything I read suggested it should raise blood sugar, not lower it, though it did not raise mine.

After my 3rd hypo--which happened after I had stopped taking Metformin long enough that it should have washed out of my system, I stopped taking Prandin. And here's where things got interesting.

For the next week--even with the Metformin completely washed out of my body--I was seeing completely normal blood sugars after eating significant amounts of carbs. As in a "high" of 105 mg/dl which I saw after eating 3 ounces of muffin.

It was only after a week that my blood sugar started creeping back up to 143 after that dose of muffin--a dose that in the past would have shot my blood sugar up to at least the 250s.

Did the Prandin "heal" me? I doubt it. Instead, my guess is that it somehow built up in my body and is taking a very long time to wash out. Since my 1 hour readings are going up slowly and my fasting blood sugar is back to where it usually is without Metformin I assume my beta cells will go back to behaving as poorly as usual.

It is possibly I was experiencing yet another of the many weird MODY things that no one knows about except other people with MODY. I have received reports of "scary hypos" with Prandin from one other person with MODY.

But given the results of the Prandin/Metformin trial reported in the Prandin Prescribing Information, maybe this effect is also happening to people with more common forms of Type 2 who take this drug combination. If it has happened to you, please post about it in the comment section of this post.

But here's what's certain: No doctor, including the endocrinologist I see, had any knowledge that Metformin and Prandin interact to dramatically lower blood sugar. Had I not been the research wonk I am I would have had no clue why I was suffering the scary hypos, and if I didn't test my blood sugar religiously, I might not even have known I was having dangerous hypos--until I ended up in an ambulance.

And nowhere on the web is there any hint that the impact of this particular drug combination can be cumulative and take many months to kick in and cause the dangerous hypos.

It took months before I started to hypo on the dose that had been giving me normal blood sugars. And eight months is twice as long as the 4 to 5 months over which the Prandin/Metformin combination was tested.

Bottom Line: Drug combinations can be very dangerous, especially as doses build up in your system. Your response to a drug or drug combination may change over time if the drug is building up in your system. With blood sugar lowering drugs this can cause very dangerous hypos. But when they do, don't expect doctors to have a clue.

September 7, 2010

Why The Latest Low Carb Scare Study is Flawed

You'll soon be hearing about a large scale epidemiological study of low carb diets and mortality published this week in Annals of Internal Medicine which purports to show that eating a low carb-meat based diet increases the incidence of mortality (i.e. death!).

Low-Carbohydrate Diets and All-Cause and Cause-Specific Mortality: Two Cohort Studies Teresa T. Fung et al. Annals of Internal Medicine September 7, 2010, vol. 153 no. 5 289-298

Here's why it's crap--and completely irrelevant to those of us who control carbohydrates to keep our blood sugars normal.

The methodology used here was this:
Prospective cohort study of women and men who were followed from 1980 (women) or 1986 (men) until 2006. Low-carbohydrate diets, either animal-based (emphasizing animal sources of fat and protein) or vegetable-based (emphasizing vegetable sources of fat and protein), were computed from several validated food-frequency questionnaires assessed during follow-up.
This raises four immediate red flags.

1.Based on Inaccurate Questionnaire Data. The standardized food frequency questionnaire used in nutrition studies is designed in such a way that it is impossible to gauge the actual food intake of people eating a true low carbohydrate diet.

It is a list of questions like, "How many times in the last month did you eat bread" followed by a multiple choice set of answers which are along the lines of "1 to 10 times" "11-25 times", "26-50" times "More than 50 times."

But the answers supplied for carbohydrate items do not allow for the possibility that the answer to a question like "How many times this past month did you eat bread" is zero or even five. Ditto potatoes. Ditto sweets.

I know first hand how inaccurate the standard food frequency questionnaire is because several years ago I was a subject in a long term study that used the standard nutritionist designed food intake questionnaire. During this time I was logging my actual food intake, with weighed portions, trying to understand my own pattern of weight loss, so I knew exactly what I was eating during any given day or month.

The nutritionist associated with the study emailed me the nutritional breakdown that I had supposedly eaten, based on my answers to the standard food frequency questionnaire. It bore no relationship at all to what I had eaten either in terms of calories or the percentages of my diet represented by protein, carbs, or fat. When I offered to send the study my actual food intake, I was told that the questionnaire they were using had been carefully validated and was standard in all nutritional studies and that there was no point in looking at what I had actually eaten.

If that isn't bad enough, the questionnaires rely on the memory of the people filling them out--who are likely to "forget" or downright misrepresent how often they ate foods they know are bad for them like sodas, snacks, and sugary desserts. It is well known that people give the answers they wish they were true on questionnaires like this where there is no way for anyone to check up on whether they are telling the truth.

Garbage in, garbage out. But since it is garbage that reinforces a religious belief nutritionists want to hold onto even though better designed studies do not support it, you will be seeing this study used to "prove" how unhealthy the low carb diet really is.

2.Misleading Definition of "Low Carb Diet" Leaving aside the fact that the data collection method renders the data highly questionable, the definition of "low carb" used in this study is almost certainly one most of us that eat a true carb restricted diet would consider a high carb diet--one of 150-200 grams of carbohydrates a day.

If that is the case, the "meat based" low carb diet was probably a "meat and potatoes and bread" diet, which we are all agree is not healthy for anyone.

3. "Meat-based diet" May Mean "Fast Food Meat and Potatoes Diet" All meats are not the same, but the standard food intake questionnaire makes no attempt to distinguish between fast food, chemical laced meat served with sides filled with trans fat and home cooked nutritious meals. The questionnaire only asks about how often the respondent ate "pork" or "beef," not where they ate it, or what cut they ate. Or most importantly, with what side dishes.

I have no doubt that eating a diet of fast food burgers (with the rolls conveniently forgotten when reporting "bread" intake") is quite capable of shortening life. But it is not because the person is eating a "meat based low carb diet" that they are risking their health.

4. "Plant based Low Carb diet" Highly Suspect The "plant based" low carb diet which was found to be so healthy here is unlikely to be low carb, since it is almost impossible to eat a true low carb diet relying on plant based foods without overdosing on soy which is far from healthy. This finding again points to the likelihood that the "low carb" diet is not low carb but moderate carb and that the plant eaters here are people who stay away from fast food outlets.

Once again, the nutritionists defending their turf use flawed methodologies to ensure that people with diabetes will continue to eat the "healthy whole grains" and sugary fruits that ensure they will end up with severe, life threatening complications.


September 2, 2010

Diabetes Does Not Create Risk Just like Having Had a Heart Attack: Another Drug Company Myth Debunked

You've probably been told that because you have been diagnosed with diabetes your risk for a heart attack is the same as that of a person who has already had one.

This turns out to be pure bullpucky.

A study published in Diabetes Care this month followed for ten years 4,410 patients aged 30–74 years: 2,260 with type 2 diabetes without coronary heart disease recruited in 53 primary health care centers and 2,150 people who had already had a heart attack but did not have diabetes.

Here's what they found:
The adjusted hazard ratios (HRs) [i.e. risk] for 10-year coronary heart disease incidence and for cardiovascular mortality were significantly lower in men and women with diabetes than in myocardial infarction patients... All diabetic patient subgroups had significantly fewer events than myocardial infarction patients.
Long-Term Cardiovascular Risk in Type 2 Diabetic Compared With Nondiabetic First Acute Myocardial Infarction Patients: A population-based cohort study in southern Europe J. Francisco Cano et al. Diabetes Care, September 2010 vol. 33 no. 9 2004-2009. doi: 10.2337/dc10-0560

Don't expect the statin drug reps to tell this to your family doctor. Selling the idea that people with diabetes "already have heart disease" has been very profitable to the drug companies. But if you've been worrying yourself sick over it, relax.

In fact, given the close relationship of post-meal blood sugar levels to heart attack incidence in all groups of people--those with and without diabetes diagnoses, it's very possible that people with diabetes who keep their blood sugars under 140 mg/dl as much as possible will have fewer heart attacks than their "healthy" peers.

You can learn more about how blood sugar level predicts heart attack far better than cholesterol levels here: A1c and Post-Meal Blood Sugars Predict Heart Attack