rops in scores all the time. Many have done it without l-arginine.

Now, how about the people who have failed to stop a rising score? Would they do better with l-arginine as part of the mix? I believe so, but sometimes we never quite know except in retrospect. It has been a great dilemma for us trying to predict from the starting gate who will or who won’t drop their heart scan score.

My view from the trenches is that l-arginine packs its greatest atherosclerosis-fighting punch in the first year or two of use, when “endothelial dysfunction” is likely to be present (abnormal artery constriction). But as all other strategies take hold—fish oil, correction of lipid and lipoprotein abnormalities, weight loss (big effect), vitamin D (another very big effect), etc.—endothelial behavior improves over time. Perhaps l-arginine becomes a less necessary component over time.

There’s no doubt that uncertainty still surrounds the use and science surrounding l-arginine. However, if you’re interested in stacking the odds in your favor, particularly during the first year or two of your plaque-reducing efforts, I think that l-arginine is worth considering. It is cumbersome, it can be expensive, some preparations may even be foul. But in the big picture of life, with hospitals trying every possible ploy to get your body on a table for a procedure, doctors perverting their mission by signing employment contracts with hospitals and agreeing to usher you into the hospital as a paying patient whenever possible, and drug companies viewing you and me as a market for medications which may or may not be helpful, l-arginine is surely not that big a burden.

Track Your Plaque and non-commercialism

If you're a Track Your Plaque Member or viewer, you may know that we have resisted outside commercial involvement. We do not run advertising on the site, we do not allow drug companies to post ads, we do not covertly sponsor supplements. We do this to main the unbiased content of the site.

We've seen too many sites be tempted by the money offered by a drug company only to see content gradually drift towards providing nothing more than cleverly concealed drug advertising. I personally find this deceptive and disgusting. Ads are ads and everyone knows it. But when you subvert content, secretly driven by a commercial agenda, that I find abhorrent.

That said, however, I do wonder if we need the participation of some outside commercial interests to help our members. In other words, many (over half) of the questions and conversations we have with people is about what supplement to take, or what medication to take. While we cannot offer direct medical advice online (nor should we) because of legal and ethical restrictions, I wonder if could facilitate access to products.

Many people struggle, for instance, with trusted sources for l-arginine, vitamin D, fish oil. Other people struggle with finding a heart scan center because of the changing landscape of the CT scanning industry. Could we somehow provide a clear-cut segment of the website that clearly demarcates what is commercial and non-Track Your Plaque-originated, yet at least provides a starting place for more info?

Ideally, we would have personally tried and investigated everything there is out there applicable to the program. But that's simply impossible at this stage.

I feel strongly that we will never run conventional ads on the site. Nor will we ever permit any outside commercial interest to dictate what and how we say something. The internet world is full of places like that. Look at WebMD. I find the site embarassing in the degree of commercial bias there. We will NEVER sell out like that, regardless of the temptation. People with heart disease are all conducting a war with the commercial forces working to profit from them--hospitals, cardiologists, drug companies, medical device companies (yes, even they advertise to the public, e.g., implantable defibrillators--no kidding). Genuine, honest, unbiased information is sorely needed and not from some kook who either knows nothing about real people with real disease, or has a hidden agenda like selling you chelation.

I'd welcome any feedback either through this Blog or through the contact@cureality.com.

The nattokinase scam

A conversation about vitamin K2 commonly leads to confusion. Several people have asked about something called nattokinase.

The scientific data on the potential role of vitamin K2 deficiency in causing both osteoporosis and vascular calcification is fascinating. Along with vitamin D3, vitamin K2 may be an important factor in regulation of calcium metabolism. Supplementation may prove to be a major strategy for inhibition of vascular calcification.

Obtaining K2 in the diet is tricky, since it's present in just a handful of foods: egg yolks, liver, traditional cheeses, and natto. This is where the confusion starts.

Natto is a Japanese fermented soy product. I've had it and it's quite disgusting. Nonetheless, Japanese who eat natto experience less fracture. (A parallel study in heart disease has not been performed.) Natto is also a source of another substance called nattokinase.

Advocates (otherwise often known as supplement distributors) claim that nattokinase is a "fibrinolytic", or blood clot-dissolving, preparation that "improves blood flow, protects from blood clots, and prevents heart attacks and strokes."

Don't you believe it. This is patent nonsense. There are several problems with this rationale:

--Any oral fibrinolytic agent is promptly degraded in the highly acid environment of the stomach. That's why all medically used fibrinolytics are given intravenously. Drug companies have struggled for years to encapsulate, modify, or somehow protect protein (or polypeptide) products taken orally from degrading this way. They've never succeeded. That's why, for instance, growth hormone (a polypeptide) remains an injection, not an oral agent. An oral growth hormone, by the way, would sell like mad, so the drug companies would very much like to figure out how to bypass the degradative effects of stomach acid. One of the "researchers" behind the nattokinase claims boasts that he has single-handedly figured out how to protect the nattokinase molecule in the gastrointestinal tract. However, he won't tell anybody how he does it. Right.

--Fibrinolytic agents are extremely dangerous. In years past, we used to treat heart attacks with intravenous fibrinolytic agents like tissue plasminogen activator, urokinase, streptokinase, and others. They have fallen by the wayside, for the most part, because of limited effectiveness and the unavoidable dangers of their use. Fibrinolytics are "dumb": they dissolve blood clots in both good places and bad. While they might dissolve the blood clot causing your heart attack, they also degrade the tiny clot in your cerebral (brain) circulation that was protective. That's why fatal brain hemorrhages, bleeding stomach ulcers, and blood oozing from strange places can also occur with fibrinolytic administration. Believe me, I've seen it happen, and I've watched people die from them.

The idea that a small dose taken orally is healthy is ridiculous. Even if nattokinase worked, why the heck would you take an agent that has known dangerous and very real consequences?

Don't let this idiocy reflect poorly on the K2 conversation, which, I believe, holds real merit and is backed by legitimate science. This is symptomatic of a larger difficulty with the supplement industry: Insane and unfounded claims about one supplement erodes credibility for the entire industry. It gives regulation-crazed people like the FDA ammunition to go after supplements, something none of us need. You and I have to sift through the nonsense to uncover the real gems in this rockpile, real gems like vitamin D3, omega-3 fatty acids from fish oil, and, perhaps, vitamin K2. But not nattokinase.

Blood pressure with exercise

Here's a frequently neglected cause for an increasing CT heart scan score: High blood pressure with exercise. Let me explain.

Paul's blood pressure at rest, sitting in the office or on arising in the morning, or at other relatively peaceful moments: 110/75 to 130/80--all in the conventional normal range.

We put Paul on the treadmill for a stress test. At 10 mets of effort (on the protocol used, this means 3.4 mph treadmill speed at 14 degree incline), Paul's blood pressure skyrockets to 220/105. That's really high.

Now, blood pressure is expected to increase with exercise. If it doesn't rise, that's abnormal and may, in fact, be a sign of danger. Normally, blood pressure should rise gradually in a stepwise fashion with increasing levels of exercise. But any blood pressure exceeding 170/90 is clearly too high with exercise. (Not to be confused with high blood pressures not involving exercise.) A handful of studies have suggested that a "breakpoint" of 170/90 also predicts heightened risk of heart attack over a long period.)

I see this phenomenon frequently--normal blood pressure at rest, high with exercise. This also suggests that when Paul is stressed, upset, in traffic congestion, under pressure at work, etc., his blood pressure is high during those periods, as well. I wouldn't be surprised to see other phenomena of underappreciated high blood pressure, like abnormally thick heart muscle (left ventricular hypertrophy), an enlarged thoracic aorta (visible on your heart scan), left atrium, perhaps even an abnormal EKG or abnormal kidney function (evidenced by an elevated creatinine on a standard blood panel).

Unfortunately, the treatments that reduce blood pressure are "stupid," i.e., they have no appreciation for what you are doing and they reduce blood pressure all the time, whether or not you're stressed, exercising, or sleeping.

Blood pressure reduction should begin with weight loss, exercise, reduction of saturated fats and processed carbohydrates (esp. wheat), magnesium replacement, vitamin D replacement. Think about CoQ10. After this, blood pressure medication might be necessary.

The message: Watch out for the blood pressures when you have a stress test. Or, if you have a friend who is adept at getting blood pressures, get a blood pressure immediately upon ceasing exercise. It should be no higher than 170/90.

Vitamin D2 vs. vitamin D3

An interesting question came up on the Track Your Plaque Member Forum about vitamin D2 vs. vitamin D3. This often comes up among our patients, as well.

Vitamin D is measured in the blood as 25-OH-vitamin D and is distinct from 1,25-diOH-vitamin D, a kidney measure, a test you do not need unless you have kidney failure.

The human form of vitamin D is cholecalciferol and is usually obtained via activation of a precursor molecule in the skin on activation by the sun. You can also take cholecalciferol and it increases blood levels of 25-hydroxy vitamin D reliably.

However, there is a cheap, plant-sourced, alternative to vitamin D3, called vitamin D2, or ergocalciferol. D2 has far less effect in the body. Taking D2 or ergocalciferol orally is an extremely inefficient way to get D. Unfortunately, it's the form often used in milk and many supplements, even the prescription form of D. About half the multivitamins and calcium supplements I've looked at contain ergocalciferol rather than cholecalciferol.

Taking vitamin D2 yields very little conversion to the effective D3. This particular issues is maddening, as the USDA requires dairy farmers to add 100 units of vitamin D to milk, and D2 is often used. In other words, the D in many dairy products barely works at all. There are many children who rely on D from dairy products who are at risk for rickets and are not getting the D they need from dairy products because of this cost-saving switch. Do not rely on milk for vitamin D for your children.

D2 or ergocalciferol is often included in the blood measures of vitamin D along with vitamin D3. The only reason it's checked with blood work is to ensure "compliance,", i.e., see whether or not you're taking a prescribed ergocalciferol. Beyond this, it has no usefulness.

25-OH-vitamin D3, or cholecalciferol, is both the blood measure and the supplement you need. This is the one that packs all the punch. Keep in mind also that it is the oil-based gelcap you want, with more consistent and efficient absorption. Tablets usually barely work at all, even if it contains cholecalciferol. Most people who take calcium tablets with D, or multivitamin with D, not only are getting a powdered form of D, but also in trivial doses. It's the pure vitamin D3, cholecalciferol, in gelcap form you want if you desire all the spectacular benefits of vitamin D.

What's that in your mouth?




Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

De Novo Lipo-what?

Humans have limited capacity to store carbohydrates. Beyond the glucose and glycogen in our blood and tissues, we have relatively little carbohydrate to draw from in time of energy need. That's why long-distance runners and triathletes have to carry sugar sources to keep blood sugar from plummeting.

Fat, of course, is different. We have virtually unlimited capacity to store energy as fat.

Because we have limited carbohydrate storage capacity, what can the body do with the excessive quantities of carbohydrates that Americans ingest? What becomes of a bagel for breakfast, wheat crackers for snacks, a whole wheat sandwich for lunch, pretzels, and whole wheat pasta that many people eat every day, not to mention the chips, soft drinks, and juices?

Excess carbohydrates are diverted to an interesting metabolic pathway called de novo lipogenesis (DNL). This refers to the liver's ability to make triglycerides from excessive carbohydrates in the diet. Triglycerides are packaged for release into the blood as VLDL. VLDL, in turn, interacts with other lipoproteins, creating small LDL particles, reduced HDL and smaller, less protective HDL. High VLDL will be measured on a standard cholesterol panel as higher triglycerides.

A University of California (Berkeley, San Francisco) group has done much of the work describing DNL.

A diet weighed towards carbohydrates, especially if 50% or greater calories are carbohydrate, is sufficient to provoke plenty of DNL, even in slender people. DNL is a big part of the reason why low-fat (and, thereby, high-carbohydrate) diets result in higher triglycerides. DNL really gets turned on many-fold if the carbohydrates are "simple," rather than "complex."

Overweight people, however, can demonstrate five-fold greater DNL even with lesser quantities of carbohydrate intake (e.g., 40% fat, 46% carbohydrate, 14% protein):





From Schwarz et al 2003. Mean (± SEM) fractional de novo lipogenesis in lean normoinsulinemic (NI), obese NI, and obese hyperinsulinemic (HI) subjects after 5 d of consuming a high-fat, low-carbohydrate diet and in different lean NI and obese HI subjects after 5 d of consuming a low-fat, high-carbohydrate diet. Values with different superscript letters are significantly different.


Excessive carbohydrates, a la standard low-fat diets, are good for nobody. The concept of de novo lipogenesis fills in a theoretical hole that now explains why people who eat carbohydrates have higher triglycerides, VLDL, and, eventually, insulin resistance and diabetes.

Gretchen's postprandial diet experiment II

I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

A wheat-free 2010

A Heart Scan Blog reader sent this fascinating description of his wheat-free adventure.

Whenever I discuss this notion of going wheat-free and the incredible health effects that develop, I invariably receive comments or emails saying something like "I eat wheat and feel fine. That can't be true." The problem is that not everybody needs to go wheat-free. 20-30% of people can include wheat in their diet and suffer little more than weight gain, some not at all.

But stories like Michael's (below) are commonplace in my experience. I've had many patients who, at first, refused to believe that wheat exposure might be the underlying cause for health struggles. But they finally give it a try and find that rashes, arthritis, acid reflux, irritable bowel symptoms, mood swings, anger, etc. are miraculously improved or gone.

Anyway, hear what Michael has to tell us:


Dr. Davis,

I want to thank you. I was browsing the web a while back and happened to stumble upon your blog post about wheat belly. The first thing that caught my attention was that I thought you had somehow gotten a photograph of me. The young man you posted an image of looked exactly like me. So I read what you had to say. After reading, I thought "Four weeks isn’t so bad. I think I can handle this."

It has now been nine weeks and all I can say is that I am completely amazed. Let me say first that twice in the past twenty years I have been tested for allergies. The first time I was tested I showed a slight reaction to Timothy Grass, but not enough to cause me any problems. The second testing I did not show a reaction to anything. So, I have always assumed that my chronic sinus problem were due to sensitivities to environmental pollutions. Now I am not so sure. I would like to list for you everything that has happened to me since I eliminated wheat from my diet.

1. I have lost a total of 12 pounds in the last 9 weeks.
2. I have lost 1 ¼ inches of belly fat
3. I have lost a tremendous amount of fat from my neck.
4. My entire life I have had problems with oily hair. I could wash my hair and three hours later I looked as if I hadn’t washed in a week. Now my hair stays clean and soft for two to three days without shampoo.
5. My hair was always flat and stringy. Now it has lots of body.
6. I used to have thick layers of dry skin on my scalp. It would come loose in chunks as large as a fingernail. That dry scalp is gone.
7. I used to have dry flaky skin that seemed to secrete oil. That no longer happens. My skin is now soft and smooth.
8. I have lived with bad acne for at least 35 years. Now it is hard to find a pimple on my body.
9. I have always had to fight dehydration. That is no longer a problem.
10. I used to drink two large cups of coffee every morning just to be able to function. I now have enough energy that I have eliminated caffeine from my diet.
11. I sleep more soundly than ever before and my dreams are clear and vivid.
12. My thought processes are more active and clear than they have ever been.
13. My chronic sinus issue is now a thing of the past.
14. I used to have problems with getting the “shakes” if I had gone more than a couple of hours without eating. It was as if I was suffering from low blood sugar. I would even be afraid that I would pass out. Now all I feel is hunger. I can go all day without eating and never feel in danger of losing consciousness.


Today is Thursday. This past Monday my wife and I were eating out and I ordered a burger without a bun. What I didn’t realize was that the burger would arrive covered in onion rings. I knocked the mountain of onion rings onto the plate but there were still a couple that were embedded in the cheese. I decided, what the hell, a couple of onion rings shouldn’t make that much of a difference. I will not make that mistake again anytime soon. Within 30 minutes I felt like there was a steel spike going through my left eye socket. I don’t remember ever being in that much pain. My sinuses were exploding. This morning, as I write this, I still feel the vestiges of that pain. Just enough that I know it is there. But after two and a half days, I am at least able to function again.

I owe you a debt of gratitude. You may have just saved my life. In the very least you have given me the means to improve my life in ways that I never thought possible.

Thank you so much,
Michael B.



Now, if wheat exposure can do that in Michael, what damage can it do in other people?

Personally, I previously experienced many of the same symptoms that Michael suffered, all gone with wheat elimination.

My advice: If you have any inkling that you might have a wheat sensitivity, make a New Year's resolution to stay wheat-free for 4 weeks and see whether you can feel any difference. Not everybody will, but many will be telling us about the dramatic health turnarounds they experienced.

Lipoprotein lipase and you

Lipoprotein lipase can make the difference between having heart disease and not having it. Having sky-high triglycerides or normal triglycerides. It can mean dinner hanging around for over 12 hours in the bloodstream, rather than the usual 4-6 hours.

If you take niacin, you must exercise

We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.


But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:





From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.

To track small LDL, track blood sugar

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.