Is there something fishy about fish oil?

To be sure, there's plenty of misinformation out there about fish oil. Take a look at the swill that passes for health information on Woman's Day: On Call with Dr. Sandy: Fish Oil and Mercury:



Reader Question: My doctor recommended that I take a fish oil supplement, but I'm concerned about mercury. Is there any way to tell which brands are lowest in mercury content?



On Call Response: When it comes to OTC supplements, the answer is no. Though most fish oil supplements sold by major brands are probably safe, there's really no way to tell what's in the bottle or how much mercury it might contain.




Perhaps Dr. Sandy should read the many independent analyses performed on nutritional supplement fish oil, including those at Consumer Lab and Consumer Report before she offers her blind criticisms.

Lovaza vs fish oil supplements?

Lovaza is the FDA-approved form of fish oil that is available only by prescription. It contains 842 mg of the omega-3 fatty acids, EPA and DHA, per capsule.

The FDA application for Lovaza is viewable here on the FDA website. Interestingly, while there is plenty of the usual regulatory gobbledy-gook about toxicology, dose escalation, and efficacy in the extensive documentation, there is little said about the issue of contamination.

In other words, critics of nutritional supplement fish oil harp on the possibility of contamination with mercury and pesticide residues, like dioxin and PCBs (polychlorinated biphenyls). Yet there is virtually nothing about these same issues in the FDA application for Lovaza.

Let's take a look at a sample over-the-counter fish oil product. Our friends at PharmaNutrients (a new Track Your Plaque partner for nutritional supplements) have a fish oil product called PharmaNutrients" Cardio. Here's an independent analysis of the Cardio product (per 1000 mg fish oil capsule):

EPA content: 566.1 mg
DHA content: 216.6 mg
(Total EPA + DHA 782.7 mg)

Cardio passed all tests for peroxides, PCBs, dioxin, furans, dioxin-like PCBs, and heavy metals (arsenic, cadmium, lead, mercury) using criteria at least 60% more stringent than European Commission (EC) standards (EC standard <2 picograms/gm for dioxins and furans, PharmaNutrients <1 picograms/gm; EC standard <10 picograms/gm for dioxin-like PCBs, PharmaNutrients <3 picograms/gm). PCBs levels in particular are less than 0.009 ppm, 90% below the industry-wide purity standard of 0.09 ppm. Likewise, mercury is >90% lower than European Commission standards.

In other words, this over-the-counter "pharmaceutical grade" fish oil has virtually nothing but omega-3 fatty acids.

Interestingly, the PharmaNutrients fish oil capsule also contains the third omega-3 fatty acid, docosapentaenoic acid (DPA), a neglected form that some authorities have proposed has superior cardiovascular protective properties over eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). If DPA is included in the analysis, PharmaNutrient's Cardio contains a total of 900 mg omega-3 fatty acids per capsule.

At some point, I'd like to see a head-to-head comparison not just on purity grounds, since I am convinced that high-quality products like Cardio can match or exceed the purity of prescription fish oil, but on efficacy in raising omega-3 blood levels, the omega-3 index. (The omega-3 index is a predictor of heart attack and sudden cardiac death--the higher, the better.) My prediction: High-quality fish oil supplements will match or exceed prescription fish oil.

More on blood sugar

Take any of the following foods:

One chicken breast
Quarter-pound ground beef
6 oz salmon steak
½ cup raw almonds
3 eggs scrambled in olive oil

How much is blood sugar increased by any item in the above list?

If you said virtually zero, you’re correct. Eat any of these foods, regardless of portion size, and blood sugar won’t change substantially. If you started with a blood sugar of, say, 90 mg/dl, 1-2 hours later it would be 90 mg/dl. It might go up or even down a few milligrams, but for all practical purposes it remains substantially unchanged.

How much is blood sugar increased by the foods in this list:

2 slices multigrain bread
1 whole wheat bagel
4 oz high-fiber breakfast cereal
2 whole grain pancakes, 2 oz maple syrup

The foods in this list are a different story from the first. Depending on your body weight, exercise habits, and other factors, a typical blood sugar response in an otherwise healthy non-diabetic person would be 120 mg/dl to 160 mg/dl. In someone with diabetes, it could easily exceed 200 mg/dl.

That isn’t good. Large blood sugar excursions to 140 mg/dl have been clearly associated with greater risk for heart attack, progression to diabetes, inflammatory responses, and other adverse health effects. In fact, blood sugars as low as 100 mg/dl after eating have been associated with increased cardiovascular risk.

Then why are the USDA, American Heart Association, the American Dietetic Association, and the American Diabetes Association telling us to eat more of the foods that shoot blood sugar up to such high levels? “Eat more healthy whole grains”?

To see how much the issue of exaggerated blood sugars after eating applies to you, a simple blood sugar check 1-2 hours after eating can show you. Either your doctor can have the test drawn or you can purchase your own inexpensive glucose meter (e.g., Walmart, Wagreens).

My prediction: You will be very surprised at blood sugar responses after common foods, including “healthy whole grains.” And, by the way, keeping blood sugar excursions to a minimum will facilitate weight loss.

Postprandial blood sugar: Almonds vs. whole wheat bread

Here's my postprandial (after-eating) blood glucose demonstration.



I tested raw almonds vs. 100% whole wheat bread, matched for calories. (Full nutritional composition below.)



Blood sugars:

Raw almonds

Start:

One-hour after eating:





2 slices 100% whole wheat bread

Start:

One-hour after eating:





100% whole wheat bread, 2 large slices

Water (g) 24.69

Energy (kcal) 158

Protein (g) 8.29

Fat, total (g) 2.14

Carbohydrate (g) 26.43

Sugars, total (g) 3.56

Fiber, total dietary (g) 4.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 0.478

Monounsaturated fatty acids, total (g) 1.022

Polyunsaturated fatty acids, total (g) 0.384





23 almonds, raw



Energy (kcal) 159

Protein (g) 5.86

Fat, total (g) 13.64

Carbohydrate (g) 5.98

Sugars, total (g) 1.07

Fiber, total dietary (g) 3.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 1.03

Monounsaturated fatty acids, total (g) 8.525

Polyunsaturated fatty acids, total (g) 3.331



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

Food sources of vitamin K2: Reprint

For some reason, my December, 2007, Heart Scan Blog post, Food sources of vitamin K2, has been receiving a lot of traffic.

I therefore reprint the vitamin K2 post below.





Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.















Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Family lessons

Lou was recovering from his 3rd bypass operation. This third go-round left him weaker, slower, less quick on the rebound. In fact, he was lucky to have survived.

At 71 years old, Lou went a good 15 years since his second bypass, another 10 years prior to his first bypass at age 46.

In the days immediately following Lou's bypass, I had a chance to talk to his son, who stayed at his Dad's bedside while Lou struggled through post-op recovery.

"Did your Dad tell you about why this has happened, what caused his heart disease?" I asked.

"Sort of. He just said I should get checked," Lou's son, Aaron, replied.

"Did he mention the lipoprotein(a) pattern he has?"

"No. He never mentioned anything like that. He just said to get checked."

That's how it gets played out more often than not: Mom or Dad has a heart attack, stents, or (3rd) bypass, the children are told to get checked. Getting "checked" assumes that the doctor knows what to check for.

In Lou's case, the reason why he was in the hospital getting his 3rd (and final) bypass was lipoprotein(a), along with genetically-determined small LDL particles, low HDL, a postprandial (after-eating) disorder, hypertension, and borderline diabetes, not to mention vitamin D deficiency, omega-3 fatty acid deficiency, and marginal thyroid function. (Lou, a retired city employee, had showed only marginal interest in correcting these patterns. While he accepted medications, he proved unwilling to engage in the diet and nutritional supplement strategies required to correct his patterns.)

So Lou's 3rd bypass operation provided a moment of reflection for Aaron to ask: "Could I share the fate of my Dad?" With Lou's combination of genetic patterns, there was at least a 75% likelihood that he did. Sadly, going to his doctor would likely yield little more than a cholesterol panel, a question about smoking, and a prescription for Lipitor.

Just getting "checked" would be, more than likely, a recipe for disaster for Aaron: heart disease in his 40s or 50s. That's why you need to take control over this sad state of affairs and ask--no, insist--that an effort be made to determine whether you might share your parents' fate.

Look like Jimmy Stewart


"This diet works great," Don declared. "But I think I've lost too much weight."

At 67 years old and 5 ft. 11 inches, Don began the program weighing 228 lbs (BMI 31.9). Because of high triglycerides, high blood sugar, high c-reactive protein, and excessive small LDL, I instructed Don to eliminate all wheat products from his diet, along with cornstarch and sweets. His intake of lean meats, eggs, vegetables, oils, raw nuts, etc. was unlimited.

Don now weighed 194 lbs, down 34 lbs over 6 months (BMI 27.1). Triglycerides, blood sugar, blood pressure, and well-being had improved dramatically; small LDL, however, had dropped only 30%--still room for improvement.

"My friends say I'm too skinny. They ask if I have cancer!"

I've heard this many times: Someone loses weight in a relatively short period of time and friends and family tell you you're too skinny. "It must be cancer. Nobody loses weight like that."

Unfortunately, many Americans have forgotten what normal looks like. Normal is certainly not a 190-lb, 5 ft 4 in woman, nor is it a 228 lb, 5 ft 11 inch man. But Americans have put on so much weight that the prevailing view of what constitutes "normal" weight has been revised upward. Normal is closer to what we see in old movies from the 1940s and '50s with people like Jimmy Stewart and Donna Reed. That's what we are supposed to look like.

So Don actually remains mildly overweight but is judged as "too skinny," or even cancer-ridden, by friends and family.

Ignore such comments. As you lose pounds and approach a truly desirable weight, realize that you are returning to the normal state, not the vision of "normal" now held by most Americans.

Getting vitamin D right

Vitamin D is, without a doubt, the most incredible "vitamin"/prohormone/neurosteroid I have ever encountered. Frankly, I don't know how we got anything accomplished in health pre-D.

Unfortunately, people I meet rarely take their vitamin D in a way that accomplishes full restoration of vitamin D blood levels. It really isn't that tough.

Here's a list of common tripping points with vitamin D:

"I take vitamin D: 1000 units a day."
This is probably the most common mistake I see: Taking a dose that is unlikely to yield a desirable blood level. (We use 60-70 ng/ml of 25-hydroxy vitamin D as our target.) Most men and women require 6000 units per day to achieve this level. There is substantial individual variation, however, with an occasional person needing much more, a rare person requiring as little as 1000 units.


"I bought some vitamin D on sale. They were white tablets."
Time and again, patients in my office who initially have had successful vitamin D replacement, despite being reminded that only oil-based forms should be taken, switch to tablets. While they initially showed a 25-hydroxy vitamin D blood level, for instance, of 67 ng/ml on 8000 units per day with an oil-based capsule, they switch to a tablet form and the next blood level is 25 ng/ml. In other words, tablets are very poorly or erratically absorbed.

I have had people use tablets successfully, however, by taking their vitamin D tablets with a teaspoon of oil, e.g., olive oil. Oil is necessary for full absorption.


"I'm going to Florida. I'll stop my vitamin D because I'm going to lay in the sun."
Wrong. 90% of adults over 40 years old have lost the majority of their ability to activate vitamin D in the skin. A typical response might be an increase in blood level from 25 to 35 ng/ml--a 10 ng increase with a dark brown tan.

There is an occasional person who, with sun exposure, increases blood levels substantially. This can occur in both fair-skinned and dark-skinned people, though I've never seen it happen in an African-American person. The occasional person who maintains the ability to convert vitamin D with sun exposure, or young people, should seasonally adjust their vitamin D dose, e.g., 6000 units winter, 3000 units summer, or some other regimen that maintains desirable blood levels. You can see that monitoring blood levels (we check levels every 6 months for the first 2 years) is crucial: You cannot know what your vitamin D needs are unless you assess 25-hydroxy vitamin D levels.


"I drink plenty of milk. I don't think I need to take vitamin D."
Oh, boy. This is so wrong on so many levels.

First of all, no adult should be drinking plenty of cow's milk. (A discussion for another day.) Second of all, cow's milk averages 70 units of vitamin D, often the D2 form (ergocalciferol), per 8 oz. Even if the FDA-mandated 100 units per day were present, an average adult dose of 6000 units would require 60 glasses of milk per day. Can you say "diarrhea"?

Likewise, other food sources of vitamin D, such as fish (300-400 units per serving) and egg yolks (20 units per yolk), are inadequate. This makes sense: Humans are not meant to obtain vitamin D from food, but from sun exposure over a large body surface area. And this is a phenomenon that is meant to occur only in the youthful, ensuring that nature takes its course and us older folks get old and make way for the young (i.e., unless we intervene by taking vitamin D supplements).


"My doctor said that my vitamin D blood level was fine. It was 32 ng/ml."

Let's face it: By necessity, your overworked primary care physician, who manages gout, hip arthritis, migraine headaches, stomach aches, prostate enlargement, H1N1, depression, etc., is an amateur at nearly everything, expert in nothing. Nobody can do it all and get it right. Likewise vitamin D. The uncertain primary care physician will simply follow the dictates of the laboratory form that specifies "30-100 ng/ml" as the "normal" or "reference range." Unfortunately, the laboratory often quotes population distributions of a lab measure, not an ideal or desirable level.

To illustrate the folly of population distributions of a measure, imagine you and I want to know what women weigh. We go to a local mall and weigh several thousand women. We tally up the results and find that women weigh 172 lbs +/- 25 lbs (the mean +/- 2 standard deviations). (That's true, by the way.) Is that desirable? Of course it isn't. Population average or population distribution does not necessarily mean ideal or desirable.


"My husband's doctor said he should take 4000 units per day. So I just take the same dose."
That would be fine if all adults required the same dose. However, individual needs can vary enormously. A dose that is grossly insufficient for one person may be excessive for another. Once again, vitamin D dose needs can be individualized by assessing 25-hydroxy vitamin levels in the blood.


"I don't need to take vitamin D. I already take fish oil."
I suspect this mistaken belief occurs either because people confuse fish oil with cod liver oil, which does contain some vitamin D. (Cod liver oil is not the best source of vitamin D, mostly because of the vitamin A content; also a discussion for another time), or because they've heard that eating fish provides vitamin D. However, fish oil capsules do not contain vitamin D unless it is added, in which case it should be prominently and explicitly stated on the label.


"I don't have to take vitamin D. It's summer."

For most people I know, if it's a bright, sunny July day, where are they likely to be? In an office, store, or home--NOT lying in the sun with a large body surface area exposed. Also, most people expose no more than 5-10% of surface area in public. I doubt you cut the grass in a bathing suit. Because of modern indoor lifestyles and fashion, the majority of adults need vitamin D supplementation year-round.


I advise everyone that gelcap vitamin D is preferable. Some, though not all, liquid drop forms have also worked. Take a dose that yields desirable blood levels. And blood levels of 25-hydroxy vitamin D are ideally checked every 6 months: in summer and in winter to provide feedback on how much sun activation of D you obtain.

If your doctor is unwilling or unable to perform vitamin D testing, fingerstick vitamin D test kits can be obtained from Track Your Plaque.

Jimmy Moore's thyroid adventure

My friend, Jimmy Moore of Living La Vida Low Carb, describes his thyroid experience here.

As Jimmy points out, he was looking for a way to jump-start a 50-lb weight loss. In my experience, low thyroid hormone levels ("hypothyroidism") are an exceptionally common cause for weight gain. Correcting even marginal hypothyroidism can facilitate weight loss, often resulting in 10 or more pounds of weight loss within the first month.

Unfortunately, Jimmy's thyroid hormone panel proved normal: TSH 1.3, thyroid hormones free T3 and free T4 in the mid- to upper-half of the reference range.

I say "unfortunately" because it is really an easy, inexpensive, and benign solution for losing weight. (I don't, of course, wish that Jimmy or anyone else develops a thyroid condition. But it really can provide gratifying weight loss results when thyroid function is low.) Jimmy might consider taking his oral temperature first thing in the morning as another means of assessing the adequacy of thyroid function.

Perhaps you will be luckier than Jimmy and have thyroid dysfunction that can be corrected and jump-start your weight loss program. Fingerstick thyroid test kits like the one Jimmy used are available here from Track Your Plaque.

The myth of mild coronary disease

I hear this comment from patients all the time:

"They told me that I had only mild blockages and so I had nothing to worry about."

That's one big lie.

I guess I shouldn't call it a lie. Is it a lie when it comes from ignorance, arrogance, laziness, or greed?

"Mild coronary disease" is usually a label applied to coronary atherosclerotic plaque that is insufficient to block flow. Thus, having a few 20%, 30%, or 40% blockages would be labeled "mild." No stents are (usually) implanted, no bypass surgery performed, and symptoms should not be attributable to the blockages. Thus, "mild."

The problem is that "mild" blockages are no less likely to rupture, the eruptive process that resembles a little volcano spewing lava. Except it's not lava, but the internal contents of atherosclerotic plaque. When these internal contents of plaque gain contact with blood, the coagulation process is set in motion and the artery both clots and constricts. Chest pains and heart attack result.

So, the essential point is not necessarily the amount of blood flow through the artery, but the presence of coronary atherosclerotic plaque. Just having plaque--any amount of plaque--sets the stage to permit plaque rupture.

One thing is clear: The more plaque you have, the greater the risk for rupture. But the quantity of plaque cannot be measured by the "percent blockage." It is measured by the lengthwise extent of plaque, as well as the depth of plaque within the wall. Neither of these risk features for plaque rupture can be gauged by percent blockage.


Coronary atherosclerosis is a diffuse process that involves much of the length of the artery. It is therefore folly to believe that a 15 mm long stent has addressed the disease. This is no more a solution than to replace the faucet in your kitchen in a house with rotting pipes from the basement up.

The message: ANY amount of coronary plaque is reason to engage in a program of prevention--prevention of plaque rupture, prevention of further plaque growth, perhaps even regression (reversal). It is NOT a reason to be complacent and buy into the myth of "mild" coronary disease, the misguided notion that arises from ill-conceived procedural heart disease solutions.


Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Red flags for lipoprotein(a)



Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque.

How do you know you have it?

Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque.

I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.

Some of the red flags for Lp(a) include:

--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present.

--HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a).

--Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a).

--Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis.

These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.

Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts.

Vytorin study explodes--But what's the real story?

The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy.

The NY Times reporting of the story:

Drug Has No Benefit in Trial, Makers Say

The 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.

The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups.

(Vytorin is the combination of simvastatin and Zetia.)

In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.

I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.)

However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco.

If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt.

Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy.

So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL?

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program:

"Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events."

Dr. Arthur Agatston in the news



The Miami Herald has a new report on Dr. Arthur Agagtston (of South Beach Diet fame) to announce his new book, The South Beach Heart Health Revolution:
The South Beach Diet doctor takes on cardio care

Agatston, the granddaddy of CT heart scanning, is always at least worth listening to. Although his diet may not be perfect, it clearly has jumped light years ahead of conventional diets like the inane American Heart Association diet. The South Beach Diet focuses on healthy oils, nuts, lean meats, vegetables, and fruits, while slashing grains (except in the often disastrous phase III).

The article lists Dr. Agatston's advice to achieve a "heart healthy" lifestyle:


• Maintain a healthy weight through diet.

• Undergo CT heart scans to check for arterial plaque.

• Do aerobic exercise, along with stretching and strengthening workouts.

• Ask your doctor about taking statins and other cholesterol-lowering drugs.


We wouldn't have CT heart scan scoring (at least in its present form) without Dr. Agatston, who developed the algorithm for scoring years ago in the early days of heart scanning. We also need to credit him with putting together a rational diet despite the counter-information emanating from the Heart Association, the USDA (a la Food Pyramid, the one that makes Americans fat and diabetic), and the American Diabetes Association, among others.

But "Ask your doctor about taking statins and other cholesterol-lowering drugs"? This is where Dr. Agatston begins to falter. While he is putting his enormous notoriety to use, his message is bland and ineffective. "Do aerobic exercise"? We don't need Dr. Agatston to tell us this.

As much as Art Agatston has added to the national conversation on heart disease and diet, he has failed to deliver the message of true heart disease prevention. His approach lacks just a few crucial ingredients like lipoprotein testing, diagnosis of hidden causes of heart disease (like Lp(a)), and vitamin D. (Two years ago I had a patient I saw for an opinion after he'd showed Dr. Agatston his lipoprotein panel. The patient said Dr. Agatston looked at the report and didn't know what to do with it and handed it back to him without comment. He then asked if he wanted his autograph.)

Anyway, the rising tide raises all boats. Agatston's repeated public endorsements of heart scans will help deliver the message that heart disease is detectable in its early stages and should trigger action to follow a heart disease prevention program.

That alone is an accomplishment in a world hell-bent on dragging us into the hospital for procedures.

Take this survey: I DOUBLE-DARE YOU

In a previous post I entitled Heart disease reversal a big "No No", I posed a challenge--a dare--to readers to ask their doctors if coronary heart could be reversed.

Here's what I said:

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.


I know of one person who actually followed through on this challenge and asked his cardiologist whether his heart disease could be reduced or reversed. As predicted, the answer was no. No explanation followed.

But allow me to reiterate: Heart disease is 1) detectable, 2) quantifiable, 3) controllable, and, in many cases 4) reversible.

What if there was a big payoff to your doctor if heart disease was reversed, say $100,000? That's enough to dwarf the payoff from procedures. Guess what? You'd have doctors fighting for your business, a chance to reverse your disease, ads to that effect, champions of reversal emerging. No new tools would be necessary. They could use the tools already available. Then why hasn't this happened? Is the technology unavailable? Are the treatments ineffective?

No, heart disease is a controllable and reversible process with tools that are available today. But there is, of course, no big payoff for doing it. So the financial incentive remains to do procedures, not to reverse the disease.

But I'd like to re-pose this challenge. Ask your doctor if heart disease can be reversed, or at least reduced. I've even posted a Survey at the top left for anyone who tries.

Again, my prediction: Nobody will try it and nobody will post survey results. Why? Despite my rantings (and those of a few others) about the concept of heart disease being a reversible process, in the public's consciousness it remains a death sentence and the only solution is hospital procedures. My colleagues continue to cultivate this attitude and it serves them well financially.

I'll be disappointed if I prove to be right. I hope that I am wrong. But I don't think that I am.



Copyright 2008 William Davis, MD

Michael Pollan on Nutritionism



The wonderfully articulate Michael Pollan has written another book. Although he presents little new to anyone who read his previous book, The Omnivore's Dilemma: A natural history of four meals, he is such a wonderful writer, with such clever ways of seeing the world, that I couldn't resist this new, less ambitious book.

The new book is In Defense of Food: An eater's manifesto.

As in Omnivore's Dilemma, Pollan reminds us that we've lost contact with real food, foods that our great grandmother would recognize, not the just-add-water, dried, pulverized, sweetened, high-fructose, hydrogenated, shrink-wrapped, artificially-colored products that pass as foods in the grocery store.

In particular, Pollan attacks what he calls the ideology of Nutritionism. "The widely shared but unexamined assumption is that the key to understanding food is indeed the nutrient. Put another way: Foods are essentially the sum of their nutrient parts." He calls this "Nutritionism."

In the section called "Nutritionism comes to market," he uses margarine as the prototypical product of this philosophy:

"No idea could be more sympathetic to manufacturers of processed foods, which surely explains why they have been so happy to jump on the nutritionism bandwagon. Indeed, nutritionism supplies the ultimate justification for processing food by implying that with a judicious application of food science, fake foods can be made even more nutritious than the real thing. This of course is the story of margarine, the first important synthetic food to slip into our diet. Margarine started out in the nineteenth century as a cheap and inferior sustitute for butter, but with the emergence of the lipid hypothesis in the 1950s, manufacturers quickly figured out that their product, with some tinkering, could be marketed as better--smarter!--than butter: butter with the bad nutrients removed (cholesterol and saturated fats) and replaced with good nutrients (polyunsaturated fats and then vitamins). Every time margarine was found wanting, the wanted nutrient could simply be added (Vitamin D? Got it now. Vitamin A? Sure, no problem. But of course margarine, being the product not of nature but of human ingenuity, could never be any smarter than the nutritionists dictating its recipe, and the nutritionists turned out to be not nearly as smart as they thought. The food scientists' ingenious method for making healthy vegetable oil solid at room temperature--by blasting it with hydrogen--turned out to produce unhealthy trans fats, fats that we now know are more dangerous than the saturated fats they were designed to replace. Yet the beauty of a processed food like margarine is that it can be endlessly reengineererd to overcome even the most embarrassing about-face in nutritional thinking--including the real wincer that its main ingredient might cause heart attacks and cancer. So now the trans fats are gone, and margarine marches on, unfazed and apparently unkillable. Too bad the same cannot be said of an unknown number of margarine eaters."


Anyone who reads and thinks a lot about nutrition will find little new here. But nobody says it better than Pollan. While Gary Taubes (Good Calories, Bad Calories) is the real thinker of our age about nutrition, Michael Pollan is the true writer about it.

With books like these making the bestsellers list, I believe that we are gradually seeing rationality return to eating. It makes people skeptical of the glitzy ads that run on TV around the clock. I hope that Pollan's new book will make more and more people leery of the latest health claim that adorn some product. "More omega-3!" "A low-fat snack." "Heart Healthy!" "High in healthy fiber!"

Cholesterol follies

Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.


So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.


If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

Equal calories, different effects

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:


VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl


HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl


Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.


What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Is skinny necessary for reversal?

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.



But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.


In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.



Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.


Copyright 2008 William Davis,MD