Too Much Vitamin D and Calcium ==> Trouble

I've been struggling with a very tough to diagnose blood pressure problem for the past six months. A lot of expensive tests came up with nothing that would explain why my blood pressure was randomly surging well into the danger zone (168/110) and refusing to respond to the medications that had always worked for me in the past.

To make it more confusing every so often my blood pressure would randomly drop back to normal and stay there for a few days so it was clear that my high blood pressure was not due to obstructed arteries or kidneys.

As so often happens, my family doctor did one round of tests and then sent me to a nephrologist who was supposed to be an expert in blood pressure. The nephrologist did another round of tests and sent me to my endocrinologist. The endo did yet another round of tests that came up blank and then told me that such cases were extremely difficult to diagnose and that my insurer would not pay for the next step which involved going to an expert at a major hospital outside of our rural region.

Fortunately, a health news item came across my screen that gave me some insight into what was going on. It described a condition called "Milk Alkali Syndrome" which after many years of nonexistence had come roaring back. The syndrome causes high blood pressure and kidney problems.

You can read about Milk Alkali Syndrome in this summary posted on Diabetes in Control:

Calcium Supplements Can Increase Risk of Kidney Failure

Though the study makes it sound as if the problem is caused by calcium supplements, close reading reveals that it caused by the combination of high calcium and high Vitamin D and that the recent spike in cases has been caused by the recent fad of people supplementing with high levels of Vitamin D.

I have been supplementing with Vitamin D for three years at my doctor's suggestion because I am a melanoma survivor and there's some data suggesting Vitamin D fights melanoma. I had achieved a level of 39 ng/ml a year ago, taking 1000 IU a day so I had raised the dose to 2000 IU because I'd been influenced by some vocal online doctors to believe that higher was better.

When I dug out my many recent lab tests I found that my family doctor had tested my calcium level. It was NOT flagged as abnormal. The range for blood calcium went up to 10.3. But even so, My blood calcium was 10.3. So while my calcium level was normal, it was just barely normal.

Further research revealed that taking diuretics (which I was doing in an attempt to lower my very high blood pressure )lowers blood calcium. So that "normal" reading was almost certainly lower than the blood calcium level I'd had a few weeks before.

Hunting for previous values I found one from before I supplemented with Vitamin D which was in the 8s. Much more normal.

I do not supplement with calcium. I stopped after reading about the Aukland Study described further on in this post). But I do eat a lot of cheese. I had already noticed that there seemed to be some link between my blood pressure and my cheese intake, but I had thought this might have something to do with a factor found in aged cheese that has also been associated with elevated blood pressure. As a result, I'd cut back on aged cheese, but not all cheese.

When I looked at my latest Vitamin D test I found it showed my Vitamin D to be 55.8 ng/dl. The test a year and a half earlier when I'd been taking only 1000 IU a day had been 39 ng/dl. My doctor had thought 55.8 an excellent level, but recent research suggests that more is not necessarily better when it comes to Vitamin D levels.

All of a sudden, my mysterious symptoms started to come into focus. I had two "normal" lab results that were no more "normal" than a 2 hour glucose tolerance test result of 139 mg/dl (a result that often ignores a one hour value well over the 200 mg/dl level diagnostic for full fledged diabetes).

When I read on further, I learned that the safe ranges for Vitamin D were drawn from studies done on White males of European ancestry--and that some data suggests that people from Non-Northern European ethnic heritages have adapted to lower Vitamin D levels and that they do poorly when they attain the high blood levels suggested for White males.

More interestingly, a decently conducted three year study of older women given high dose injections of Vitamin D to avoid osteoporosis discovered that levels of blood Vitamin D corresponding to mine correlated with more not less bone fractures. You can read that study here:

Annual High-Dose Oral Vitamin D and Falls and Fractures in Older Women: A Randomized Controlled Trial. Kerrie M. Sanders. JAMA. 2010;303(18):1815-1822.

(Note that the units used in this study were nmol/L not the ng/dl labs use in the United States. Converting the units shows that these women started out deficient with average Vitamin D levels of 19.63 ng/dl, but after the Vitamin D shots their levels went up to an average 48.08 ng/dl.) We know that too much blood calcium is linked with bone brittleness, too.)

Another recent study, The Aukland Study, had found that women supplementing with calcium had more heart disease (presumably linked to calcification in their arteries) than women who didn't.

Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Mark J Bolland. BMJ. 2008;336:262-266 (2 February), doi:10.1136/bmj.39440.525752.BE (published 15 January 2008)

And a disturbing comment in yet a brand new study commenting on the Aukland Study really got me thinking.

It said:

there is substantial epidemiological evidence that serum calcium levels in the upper part of the normal range are a risk factor for vascular disease

The combination of this information with the information that Milk Alkali syndrome (high blood calcium caused by high calcium and Vitamin D intake) caused high blood pressure suggested to me that I might have found the explanation for my blood pressure problems--and that I had been, once again, the victim of another doctor-caused medical disaster!

Once I had sorted this out, I stopped taking the 2000 IU a day of Vitamin D I had been taking for the past year. I cut out all cheese from my diet--which made me realize just how much cheese I'd been eating--much more than I thought!

I had read it takes about 2 weeks to eliminate HALF the excess vitamin D in the blood and that more Vitamin D is stored in fat and slowly released, so I figured it would take a while to restore truly normal calcium levels. Even so, after ten days it looks like I might be onto something. My blood pressure has already come down--it's in the 120s over 80s rather than the 140s over 90s when I wake up and has been staying in that range most of the day instead of spiking higher.

I will be avoiding cheese for another month and tracking how my blood pressure does. When I see my endo for my regular appointment in October I'll ask for repeat Calcium and Vitamin D tests. Since I did well at the 39 ng/ml Vitamin level I'll shoot for that--but only if I can sustain that level without elevated calcium. Meanwhile, I hope I haven't inadvertantly deposited damaging amounts of calcium in my arteries and kidneys.

WHAT DOES THIS MEAN FOR YOU?

For those of you reading this who have been supplementing with Vitamin D thanks reading all the doctor-inspired hype, my message here is NOT that you should not take Vitamin D.

Instead, what I'm saying is that if you are supplementing Vitamin D you need to get your blood levels of both Vitamin D and Calcium tested periodically so you can avoid dangerous Calcium levels. 1000 IU appears to be a safer level for supplementation than anything higher, and if you don't know what your levels are you should not supplement with more until you can check those levels out.

My other point is this: if you are eating a low carb diet and also taking white, chalky pills--prescription or other supplements), be aware that you may be getting much more dietary calcium than you realize.

Since it is looking like high normal calcium levels damage both your arteries and kidneys maintaining truly normal calcium levels is probably most important than obsessing about cholesterol.

UPDATE 8/5/10: Two months after stopping ALL Vitamin D supplementation and avoiding cheese my calcium levels are back to normal and my blood pressure is far more stable. I'm gong to stick with this regimen for a few more months and only supplement D in the fall after I stop gardening each day. I'll stick with the 1000 IU level which worked well for me in the past.

 

Yet More Good News About Metformin

Sometimes it seems like every day brings us new bad news about the side effects associated with the expensive, new heavily promoted diabetes drugs that most doctors push on patients.

And then there's metformin. We keep getting news about metformin's side effects, but for the past year every single on of those side effects has been something good, for example, we now know metformin decreases the risk heart attack and also of contracting several important cancers.

Now scientists have found that metformin has yet another positive side effect: it blocks the reproduction of the Hepatitis C virus which allows people infected with it to recover from this dreadful disease.

You can read the details here: Science Daily: New Use for Old Drugs in Treating Hepatitis C

Given that you can buy a month's worth of generic Metformin for $4 at many pharmacies you won't hear much about this. No one gets rich selling you generic metformin so no one sends out the press releases. Your doctor may not hear about this either.

But if you are someone who, like me, thinks long and hard before popping a pill because you know how dangerous so many pharmaceuticals have turned out to be, this latest piece of news should reassure you that metformin--which lowers blood sugar, stops the liver from dumping glucose, and helps muscles and liver burn fat--is one drug you can take knowing that its side effects make it fight other dangerous diseases and keep you living a longer and healthier life.

The Latest Avandia Outrage: A Shockingly Bad Study Promotes It for Prediabetes

The slimy weasels who profit from selling the dangerous drug Avandia don't give up easily. Though there is incontrovertible evidence that their drug causes heart failure in people who did not have it before starting the drug, as well as ostoporosis and an increased risk of heart attack, they keep sending the health media carefully doctored press releases touting new and marvelous features of their drug.

The latest is the claim that Avandia does a humdinger of a job at preventing diabetes, reducing it by two thirds. The study is a triumph of sleazy research technique, but because the drug reps will be hard at work "teaching" your doctor of this wonderful new feature of their dreadful drug, you need to understand what the study actually did and what it learned.

The study abstract can be found here:

Low-dose combination therapy with rosiglitazone and metformin to prevent type 2 diabetes mellitus (CANOE trial): a double-blind randomised controlled study. Prof Bernard Zinman. The Lancet. June 3, doi:10.1016/S0140-6736(10)60746-5

As you can see by looking at the title, this study combined Avandia with Metformin. Because we know that Metformin delays the diagnosis of Type 2 diabetes (by lowering blood sugar, not by correcting underlying flaws) you'd assume that any trial of metformin with another added drug would compare the combination with metformin alone.

But since the point of this study was to breath life into the decaying corpse of Avandia, that comparison was omitted. There are only two groups in this study, those on the Avandia metformin combo and those on a placebo.

Beyond that, the study involved only about 200 people, divided into two groups. This means that if one out of every two hundred people taking Avandia developed a severe or even fatal complication, the study group is too small to detect it. Since the problem with Avandia is that it has been shown in large studies to cause severe and sometimes fatal complications the study design used here is worthless and very clearly designed only to squeeze more profit out of GlaxoSmithKline's dangerous drug.

The next problem with the study is that it lasted only a median of 3.4 years. Why is this a problem? Because even if the study size had been big enough to make the severe side effects evident, the most serious of the Avandia side effects may take up to a decade to become evident. That is because Avandia works by transforming bone stem cells into baby fat cells into which glucose gets pushed. (That is why Avandia causes permanent weight gain.) This means that over time bones are weakened because they don't get new bone cells coming in to reinforce them. Eventually they start to crack and by then it is too late to fix the problem. But you won't see this effect over 4 years. So again, this study was designed to avoid highlighting a known damaging side effect of Avandia.

But setting aside the fact that it is impossible to know from this study whether Avandia is safe in this context, the actual finding of the study was another blow to Avandia's claims, and makes it crystal clear why there was no "metformin only" group included in the study--though you wouldn't know this from the press coverage.

The study claims,

70 (80%) patients in the treatment group regressed to normal glucose tolerance compared with 52 (53%) in the placebo group (p=0·0002).

Note that the study is reported as claiming that two thirds of those who took Avandia (with metformin, though the headlines miss that) did not progress to diabetes. But at the same time, more than one half of those who did not take any drug also reverted to normal blood sugar status. So in fact, the drug combo only kept an additional 27% of participants from being diagnosed with diabetic blood sugars.

Note that DPPT--a far more robust study of 3234 people with pre-diabetes found that Metformin alone decreased the progression to diabetes by 31% over an average of 2.8 years.

Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or Metformin:Diabetes Prevention Program Research Group NEJMVolume 346:393-403, February 7, 2002, Number 6

So there is basically no significant difference in effect between the use of metformin alone and metformin combined with dangerous drug Avandia even allowing for the extra couple months in the Avandia study.

All this seems to have eluded the peer reviewers who approved this study for publication.

Okay, that's bad enough, but there's one last point. The makers of Avandia promote it to doctors with the claim--unsupported by evidence--that members of the TZD drug class to which it belongs rejuvenate beta function. This study, like every other study of the subject finds that isn't true. The Lancet study states,

The change in β-cell function, as measured by the insulin secretion-sensitivity index-2, did not differ between groups (placebo −252·3, −382·2 to −58·0 vs rosiglitazone and metformin −221·8, −330·4 to −87·8; p=0·28)

So the improvement achieved in the drug group (most likely from taking the metformin) did not occur because the beta cells were functioning better, but only because blood sugar was lowered. Whether this was because the metformin blocked liver dumps, or because it promoted glucose uptake at the muscles by revving up AMP-Kinase, or because Avandia pushed excess glucose into brand new baby fat cells is unknown.

So that's the story that the folks at The Lancet somehow missed. And because they missed it, you can be sure some percentage of boneheaded doctors will read this new study and put patients who don't have diabetes on Avandia. After all, why prescribe an effective, safe, generic drug that can be bought for $4 a month--Metformin--when you can prescribe one that does nothing but harm and costs up to $100 a month? The answer has a lot to do with the subtle incentives drug companies still provide doctors, but that's the subject for another blog post.

Unfortunately, even doctors who are gun shy about Avandia still believe that its evil twin Actos is safe. It isn't. Actos also causes heart failure and works by changing bone baby cells into baby fat cells causing permanent weight gain and, long term, damaged and broken bones. Actos may not cause heart attack, but that information won't mean much if you develop heart failure, which over time is just as fatal. It's also worth noting both drugs raise the risk of retinal edema which means that if you are particularly unlucky, both Avandia and Actos can seriously damage your vision.

Bottom line: If you have pre-diabetes can't get your blood sugar back to normal by cutting carbs (which has been proven far more effective than any drug) stick with metformin. It's safe, it works, and its side effects include things like weight loss and a lower incidence of cancer.

What the Health Media Missed: JAMA Study Quantifies Reporting Spin

If you have been reading this blog for a while, you know that from time to time I pick out some company funded study that has turned into a media sound bite promoting the company's product and read it to see what it really found. Almost always close reading of these studies finds statistical abuse so blatant that one concludes that the peer reviewers who approved it for publication flunked Statistics 101.

Now a study in JAMA quantifies just how bad this statistical abuse really is. The study is,

Reporting and Interpretation of Randomized Controlled Trials With Statistically Nonsignificant Results for Primary Outcomes. Isabelle Boutron et al. JAMA 2010;303(20):2058-2064.

A "statistically nonsignificant result" is one that could be due entirely to chance. If I test the proposition that a coin toss is more likely to come up heads by tossing a coin five times no combination of heads and tails that emerges from this "experiment" would be statistically meaningful. You have to toss that coin a lot more times to get a meaningful result because the same coin that would come up heads 50% of the time over 1,000 coin tosses may easily come up heads three or even four times when tossed only five times.

So what this JAMA study was examining was how researchers reported studies in which the hypothesis being tested came up with a statistically meaningless result, for example, a study that asks whether Drug X decreases the number of heart attacks in some population which finds that the change in the number of heart attacks in the study group could be entirely due to chance.

What the JAMA study found was that in 72 studies where the primary outcome resulted in a statistically nonsignificant result there was significant "spin."

Spin was defined thus:

...specific reporting strategies, whatever their motive, to highlight that the experimental treatment is beneficial, despite a statistically nonsignificant difference for the primary outcome, or to distract the reader from statistically nonsignificant results

In plain English, "spin" means claiming some treatment works when the statistics show it does not.

How frequent was spin? The JAMA Study finds:

The title was reported with spin in 13 articles (18.0%)

Spin was identified in the Results and Conclusions sections of the abstracts of 27 (37.5%) and 42 (58.3%) reports, respectively, with the conclusions of 17 (23.6%) focusing only on treatment effectiveness.

Spin was identified in the main-text Results, Discussion, and Conclusions sections of 21 (29.2%), 31 (43.1%), and 36 (50.0%) reports, respectively.

More than 40% of the reports had spin in at least 2 of these sections in the main text.

So no, I am not paranoid when I assert that peer reviewers approve the publication of studies that claim results where none occurred, based on ignorance of how statistics work.

Some of the ways I've seen this kind of spin deployed are to report a study as showing that results "trended" towards the desired outcome. In the case of our coin toss, the coin tossed five times that comes up heads three times "trends" towards heads. This is meaningless, since if you toss it 1,000 times it comes up 50% heads and 50% tails.

When a drug "trends" towards reducing heart attacks because 103 people who took the drug had heart attacks while 105 people who didn't take the drug had heart attacks, you have the identical meaningless finding. You would need to see a much bigger difference in outcomes to determine that the drug was effective when testing it in such a small group.

But using the "trend" argument is a very common way that drug companies and supplement companies suggest to the statistically ignorant (including the peer reviewers) that their product works when it doesn't.

This is why so many claims made for years about vitamins, supplements and new drugs turn out to be wrong when someone attempts to confirm the result with a large, statistically meaningful study.

Beyond mistating the study result, a common strategy for a company trying to spin gold out of dross is to misapply a statistical technique to the meaningless result that amplifies it into a number that appears, to those who don't understand the GIGO principle, to be meaningful.

When there is a statistically meaningless finding for incidence of heart attack, use the inflationary measure, "risk of heart attack," and if that still doesn't give you a meaningful statistic, try measuring "change in risk." If risk (already a statistical amplification of incidence) drops a meaningless 2% in the drug group and 1% in the placebo group, we have a 50% "change in risk." That sounds very impressive to the math-flunkees who decide which studies get published, because I keep seeing just that kind of statistical slight of hand being used. But it is meaningless, because since the difference in incidence could be entirely due to chance and come out the other way if the study was repeated again any statistic derived from incidence is statistically meaningless, too.

This doesn't even get into the related issue that drug companies falsify results or run "controlled trials" where the two groups under study are not well matched. If you compare a sicker older placeo group to a younger healthier group who take a drug, your drug may look effective when it isn't.

And then, there is the issue of "controlling" for various cofactors. The notorious ACCORD study, long interpreted as meaning that tight control killed people with diabetes ignored the fact that the people in the tight control group who experienced bad outcomes did not, in fact, have tight control. There were more people with bad control in the "tight control" group than in the control group, so the slight increase in bad outcomes in that "tight control" group had nothing to do with tight control but was instead due to LACK of tight control.

Sadly hundreds of thousands of people with diabetes have been told by now that "tight control" is dangerous and that they should maintain A1cs of 7%, not 6% to be "safe." It will take years to undo the damage because busy health professionals don't have time to read all the health news and the debunking of ACCORD did not get the press that the original study received.

BOTTOM LINE: Your health and safety is being severely compromised by the peer reviewers who rubber stamp publication of company sponsored research that pretend that statistically meaningless results have meaning. The people who pay for this deceit and stupidity are the patients who end up taking expensive, dangerous, and worthless drugs.

Sadly, in a society that remains mostly math-illiterate, this isn't going to change any time soon.

Understanding Fasting Blood Sugar

Among the most common questions people have about Type 2 diabetes is this: how can they lower their fasting blood sugar?

To answer this question in a way that will help you lower your blood sugar we are going to have to first explain why doctors measure fasting blood sugar and what it does--and does not--tell us about our blood sugar health.

WHAT IS FASTING BLOOD SUGAR?

Traditionally, fasting blood sugar is the value you get when you test your blood sugar after an 8 hour long fast--which is usually immediately upon waking. In a normal person this fasting blood sugar would also be the "baseline" blood sugar--the level to which blood sugar returns a few hours after every meal all day long.

However, for reasons we will discuss later on, this is often NOT the case for people with Type 2 diabetes, whose morning blood sugars may be much higher than the baseline level they achieve after meals for the rest of the day.

Doctors have for decades relied on the FPG (fasting plasma glucose) test which measures fasting blood sugar to diagnose diabetes. The reason for this is NOT that FPG test results predict diabetic complications. They don't. Post-meal blood sugar tests are a much better indicator of whether a person will get the classic diabetic complications, and the A1c test is a better indicator of potential heart disease.

But the FPG test is cheap and easy to administer, hence its popularity.

The value most of us would find much more helpful in assessing our health is not fasting blood sugar but something else: the number of hours a day our blood sugar spends elevated over the level known to cause complications, which is roughly 140 mg/dl (7.7 mmol/L).

A person can wake up with a FPG of 130 mg/dl (7.2 mmol/L), but if it drops after breakfast and most hours of the day are spent with blood sugars that remain under 120 mg/dl, the person can expect years of complication-free living.

In contrast, a person may wake with a normal FPG of 98 mg/dl (5.4 mmol/L) but end up spending the next 14 hours with blood sugars well over 170 mg/dl (9.4 mmol/L). That person is seriously at risk for heart disease, diabetic nerve damage, kidney damage, and retina damage.

So when you assess your own fasting blood sugar, the question you want to ask is this: How many hours a day am I spending with my blood sugar in the range that causes complications? Not, necessarily, how can I lower my fasting blood sugar?

Obviously, if your fasting blood sugar is over 140 mg/dl (7.7 mmol/L) and goes up after each meal, you are going to be spending many hours a day in the danger zone and lowering your fasting blood sugar does become a huge issue. Fortunately, it is also one that can be solved.

WHAT RAISES FASTING BLOOD SUGAR?

Several independent factors can raise fasting blood sugar, and if you have a problem with it, the reason for your problem may NOT be the same as the reason for another person's even if they get the identical blood test results that you get.

Here are common reasons for high fasting blood sugar.

1. High post meal blood sugars. Your beta cells can only make so much insulin. If you elevate your blood sugars severely by eating more carbohydrate than your body can handle, your body will spend the whole night using what insulin it can manufacture to mop up the glucose that is still circulating thanks to those high carb meals.

Many people with diabetes cannot handle more than 12-20 grams of carbohydrate at a single meal, no matter what you might have been told by doctors or dietitians. Many of us will find that if we drop our carbohydrate intake dramatically, our fasting blood sugar plummets equally dramatically. It may take as little as two weeks of restricted carbohydrate intake to see fasting blood sugars revert to normal.

You can use this technique to lower your fasting blood sugar. It has worked for literally thousands of people:

How to Get Your Blood Sugar Under Control

2. Damaged Basal Insulin Secretion. The body secretes insulin in two different physiological processes which are described on this page: How Blood Sugar Control Works--And How It Stops Working. I urge you to read this page because mastering the concepts it explains will greatly help you understand and manage your diabetes.

Basal insulin secretion takes place throughout the day without reference to what you eat. Tiny amounts of insulin are squirted into the blood stream in small pulses every few minutes. However, sometimes things go wrong with the factors that control basal secretion. If that happens, your body may still be able to secrete insulin in response to meal time rises in glucose, but you lose the ability to secrete those tiny pulsing bursts. This can cause a rise in fasting glucose that can not be corrected with dietary changes. If you have this problem, you might need a basal insulin--a slow acting insulin that mimics the effect of natural basal secretion.

Basal failure is relatively rare, but when it happens you often find people with high fasting blood sugars whose blood sugar normalizes as soon as they eat and stays normal until they have metabolized their last meal. There are also genetic forms of diabetes (GCK mutations) that will cause elevated fasting glucose, however, this will be a lifelong problem, not one that comes on with age.

3. Dawn Phenomenon. If your blood sugar is highest first thing in the morning, and normalizes after you eat or exercise and stays normal hours after dinner, you may have a disturbance of regulatory hormones that is called "dawn phenomenon."

Our bodies prepare for waking up by secreting stimulating hormones shortly before dawn. These increase our insulin resistance in order to raise blood sugar a small amount. If we were animals who had to go hunt for our first meal, that excess glucose would be useful. Since were are people with refrigerators, it is less so.

Everyone experiences this early morning hormone burst, but in people with diabetes it can become highly exaggerated. In some people it is resistant to any treatment, but once the person goes about their day and eats, the blood sugars become more controllable.

If you have dawn phenomenon that doesn't respond to various lowering techniques, don't panic. As long as you are spending most of the day with your blood sugars at a safe level (Always under 140 mg/dl and under 120 mg/dl as much as possible) you'll be fine.

4. Too Much Injected Insulin or Oral Insulin-Provoking Drug. This is counter-intuitive, but common. If you are using a basal insulin (Lantus or Levemir) there is a temptation to use a lot of it to try to lower post meal blood sugars. Your sugars will be pretty good as long as you keep eating carbs, but once you stop eating at night, the insulin keeps being absorbed into your blood stream and by 3 AM it is quite common to hypo.

However, many of us as soon as we hypo slightly, experience a burst of counterregulatory hormone intended to push the blood sugar back up to normal so by the time you wake your blood sugar is high, not low. You can tell if you have had a counterregulatory burst because it will often wake you up at 3 AM with a jolt. Your pulse will be fast and your blood pressure may be elevated too. If you measure your blood sugar it won't be low, because as soon as you get that jolt, your blood sugar will surge. That's what the jolt is meant to do.

If you are waking at 3 or 4 AM and end up with high fasting blood sugars, cutting back on your Lantus or Levemir may solve the problem. Lantus and Levemir are NOT meant to cover the carbohydrates you eat at meals, only to lower your baseline blood sugars. If you need insulin to control meals, you need to ask your doctor for fast acting insulin and the diabetes education it requires to learn how to use it correctly.

Glipizide and Amaryl (glimepiride) can also cause this problem as they cause long lasting insulin secretion in people who are sensitive to them.

5. Too Much Blood Pressure Medication. Too much blood pressure medication will also cause an early morning counterregulatory attack because if your blood pressure drops too low, you will get a burst of epinephrine and other hormones meant to keep you alive. It will raise both blood pressure and blood sugar.

I experienced this myself and since posting about it on my blog have received emails from others who experienced this same phenomenon. It is most likely if your blood pressure medication is giving you low normal readings during the day--90/60 for example, or if you experience postural hypotension attacks where you black out when you bend over.

USEFUL TECHNIQUES FOR LOWERING FASTING BLOOD SUGAR

Here are some of the things people report helped them. They are worth a try.

1. Cut way back on your meal-time carbohydrate intake.

2. Drink a glass of wine with dinner or before bedtime. One is enough. The alcohol can inhibit the liver from dumping glucose.

3. Eat a protein snack before bedtime.

4. Change the time of day when you take your medications. Metformin ER taken at bedtime will have a stronger impact on fasting blood sugar than the same pill taken in the morning. However, you may see higher post meal values if you change the timing. Remember your goal is maximum hours of lower blood sugar, not one low reading in the morning.

5. Split Lantus or Levemir doses so you take half in the morning and half in the evening. Lantus does not last 24 hours in many people, especially when taken in small doses (12-30 units) so if you take it in the morning it may be gone by 3 AM. Splitting the dose may give you better coverage. Discuss this with your doctor before you make changes, especially if you haven't been taught how to adjust your insulin doses. DO NOT MODIFY YOUR INSULIN DOSES IF YOU DON'T UNDERSTAND HOW THEY WERE SET!

6. Metformin. If you aren't taking metformin, ask your doctor about it. It is the most appropriate drug for controlling fasting blood sugars because it can sometimes block the liver dumping that raises blood sugar in response to dawn phenomenon hormones.