Heart scan gone wrong

Those of you reading the Heart Scan Blog, I hope, have come to appreciate the power in measuring atherosclerotic plaque, the stuff of coronary artery disease, and not relying on indirect potential "risk factors," especially the fictitious LDL cholesterol.

However, like all things, even a great thing like heart scans can be misused. Here's a story of how a heart scan should NOT be used, submitted by a reader.


Dr. Davis,

First of all, let me start out by commending you on all of the work you are doing with your website, blogs, etc. You are truly a breath of fresh air at a time when conventional medicine is no longer making any sense. In the last 3 years or so, I have spent a lot of time using the internet to try and find answers . . . and just about every time, when I find things that make "sense," it coincides which the recommendations you provide. Thank You!!

I am 56 years old, and roughly 5 years ago I bought your book, Track Your Plaque, primarily because I had asked my then Internal Medicine physician about why we weren't more "proactive" about determining the state of our cardiovascular health...since the means to do so existed (scans). He was trying to get me to go on a statin because my cholesterol #'s were a little high and at the time I smoked. Other than that, I was in perfectly good health with no side effects or issues. The following year at my annual physical, we again discussed this and he gave me a few options and I ended up having a calcium score done, which showed some blockage, but again, I never had any pains, sweats, or any other symptoms whatsoever, and I am a very active former athlete. This is when I bought your book to try and set a course of plan that wouldn't just include pharmaceuticals.

At the same time, my father was in his last months of life dealing with prostate cancer and the multiple radiation and chemo treatments, so I was making many trips from my home to be with him . . . a 4 hour drive, and very disruptive to family, as I still have 3 kids at home. At what I thought was going to be my last visit with him, I stopped at the cemetery he had planned on being buried to confirm details and such and then started home.

As I was driving, a symptom hit me which I was unfamiliar with (pretty sure it was an anxiety attack now) and I stopped at a friend's house in Chicago, as I didn't want this to be a heart attack while I was driving. This is when I began thinking about the heart scan and the blockage, and ended up driving back later that night and went right to the ER....not because I had any chest pains, but thought it best to be checked out because I did not want to go before my dad did. I ended up staying the night. In the morning the cardiologist PA [physician's assistant] came in with a copy of my calcium scoring and said it was best to have a heart cath...which I was in total agreement with since it would definitively tell me the current condition of my coronary vessels. As I was getting ready to be wheeled into the cath lab, they approached me with a form that would allow them to treat (stent). This is where I became very uncomfortable, in that I had never even met the cardiologist . . . and I didn't like this. No one ever had asked if I was experiencing pains or anything else . . . but I buckled and signed the form.

Before you knew it, I was awake watching my heart being cathed and the cardiologist angry because they did not have all the right sizes of stents, so he had to use a couple extra and I ended up w/5 total . . . and my life changed forever! In looking back, I can't necessarily argue the need for intervention, but in hindsight, it would have been nice to have tried an alternative method of reversing my plaque, especially since I had never experienced any symptoms and didn't appear to be in any imminent danger.

Upon release from the hospital I was put on a cocktail of drugs that typically follow and I then began to search and research. No one talked to me about lifestyle changes other that smoking....but nothing on diet or other means of cholesterol control, etc....in fact, when I had to pick out my meals in the hospital, they wouldn't let me have cheese....but the rice crispy treat was fine....how stupid! They originally told me the Plavix had to last 6 months....and then 12....and then 2 years....I stayed on it for 1-1/2 years and it was the only thing other than a baby aspirin. I went to another cardiologist out of town and he wanted me back on 5 or 6 medications and said that now I had the stents....I would have to be on these for life.....and he was the expert that talked at several main conferences.....my last trip to him.

Now, fast forward to about 6 months ago: I was participating in a father-son soccer scrimmage and was playing goalie. It was wet out and I couldn't catch very well. So being the competitive person I am, I resorted to using my chest on several of the saves and also took a direct blow to my eye ( I wear glasses) and the eye started swelling up pretty good. We then finished and went inside to have pizza and everyone was concerned about my eye. About 30 minutes later I excused myself as i felt some pretty significant sweats and subsequently a pretty severe pain directly in the middle of my chest....I was having a heart attack! Called 911 and went to hospital (2-1/2 years since original stents) and my local cardiologist removed the blockage that was at the anterior portion of my 1st stent causing the blockage. The huge disappointment to me is that I had taken many steps to improve my overall health. But now that I have foreign bodies in my vessels, the chance of further clotting is something that i will most likely always have to live with.

BU, Michigan



This is an example of how heart scans should NOT be used. They should NEVER be used to justify a procedure, no matter how high the score or where the plaque is located. The "need" for procedures is determined by symptoms (BU's symptoms were hardly representative of heart disease), blood findings, EKG, stress testing, and perhaps CT coronary angiography. "Need" for procedures can never be justified simply on the basis of the presence of plaque by a heart scan calcium score.

Unnecessary procedures like the one BU underwent are not entirely benign, as his experience at the soccer game demonstrated.

Heart scans are truly helpful things. But, like many good things, they are subject to misuse in the hands of the uncaring or greedy.

Blood sugar: Fasting vs. postprandial

Peter's fasting blood glucose: 89 mg/dl--perfect.

After one whole wheat bagel, apple, black coffee: 157 mg/dl--diabetic-range.

How common is this: Normal fasting blood sugar with diabetic range postprandial (after-eating) blood sugar?

It is shockingly common.

The endocrinologists have known this for some years, since a number of studies using oral glucose tolerance testing (OGTT) have demonstrated that fasting glucose is not a good method of screening people for diabetes or pre-diabetes, nor does it predict the magnitude of postprandial glucose. (In an OGTT, you usually drink 75 grams of glucose as a cola drink, followed by blood sugar checks. The conventional cut off for "impaired glucose tolerance" is 140-200 mg/dl; diabetes is 200 mg/dl or greater.) People with glucose levels during OGTT as high as 200 mg/dl may have normal fasting values below 100 mg/dl.

High postprandial glucose values are a coronary risk factor. While conventional guidelines say that a postprandial glucose (i.e., during OGTT) of 140 mg/dl or greater is a concern, coronary risk starts well below this. Risk is increased approximately 50% at 126 mg/dl. Risk may begin with postprandial glucoses as low as 100 mg/dl.

For this reason, postprandial (not OGTT) glucose checks are becoming an integral part of the Track Your Plaque program. We encourage postprandial blood glucose checks, followed by efforts to reduce postprandial glucose if they are high. More on this in future.

Diabetes from fruit

Mitch sat in my office, looking much the same as he had on prior visits.

At 5 ft 7 inches, he weighed a comfortable 159 lb, though he did have a small visible "paunch" above his beltline.

I had been seeing Mitch for his heart scan score of 1157 caused by low HDL of 38 mg/dl, severe small LDL (87% of total LDL), and lipoprotein (a).

Part of Mitch's therapeutic program was elimination of wheat, cornstarch, and sugars, the three most flagrant triggers of small LDL particles, and weighing his diet in favor of oils and fats to reduce Lp(a). However, Mitch somehow failed to follow our restriction on fruit, which we limit to no more than two 4 oz servings per day, preferably berries. He thought we said "Eat all the fruit you want." And so he did.

Mitch had a banana, orange, and blueberries for breakfast. For lunch, along with some tuna or soup, he'd typically have half a melon, a pear, and red grapes. For snacks, he'd have an apple or nectarine. After dinner, it wasn't unusual for Mitch to have another piece of fruit for dessert.

Up until Mitch's last visit, he'd had blood glucose levels of 100-112 mg/dl, above normal and reflecting mild insulin resistance and pre-diabetes. Today, on his unlimited fruit diet, his blood sugar: 166 mg/dl--well into diabetes territory.

I helped Mitch understand the principles of our diet better and advised him to reduce his fruit intake to no more than the 2 small servings per day, as well as sticking to our "no wheat, no cornstarch, no sugar" principles.

While fruit is certainly better than, say, a half-cup of gummy bears (84.06 g carbohydrates, 50.12 g sugars), fruit is unavoidably high in carbohydrates and sugars.

Take a look at the carbohydrate content of some common fruits:

Apple, 1 medium (2-3/4" dia)
19.06 g carbohydrate (14.34 g sugar)

Banana, 1 medium (7" to 7-7/8" long)
26.95 g carbohydrate (14.43 g sugar)

Grapes, 1 cup
27.33 g carbohydrate (23.37 g sugar)

Pear, 1 medium
25.66 g carbohydrate (16.27 g sugar)

Source: USDA Food and Nutrient Database

Fruit has many healthy components, of course, such as fiber, flavonoids, and vitamin C. But it also comes with plenty of sugar. This is especially true of modern fruit, the sort that has been cultivated, hybridized, fertilized, gassed, etc. for size and sugar content.

When you hear such conventional advice like "eat plenty of fruits and vegetables," you should hear instead: "eat plenty of vegetables. Eat a small quantity of fruit."

The sniff test

It is well established that omega-3 fatty acids from fish oil are free of mercury, PCBs, furans, and other pesticide residues. Several independent analyses have all agreed: little to none are contained in fish oil. In the Consumer Lab series of assessments, for example, no fish oil supplement failed because of any heavy metal or pesticide residue.

However, oxidative byproducts are a problem. Just as fish that sits on the store shelf or your refrigerator too long starts to smell "fishy," so will fish oil. When fish or fish oil becomes rancid, smelling like rotten fish at its worst, it means that

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
All posts by william-davis

CIS: Carbohydrate intolerance syndrome

Carbohydrate intolerance comes in many shades and colors, shapes and sizes.

I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)

At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc.

An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl.

This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all.

Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.

How about Kevin?

Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:

HDL 36 mg/dl
Triglycerides 333 mg/dl

BP 132/78
Waist circumference 34 inches
Blood sugar 98 mg/dl

Kevin meets the criteria for metabolic syndrome on only two of the five criteria and therefore does not "qualify" for the diagnosis.

Kevin's basic lipids showed LDL 170 mg/dl, HDL 36 mg/dl, triglycerides 333 mg/dl.

But take a look at his underlying lipoprotein patterns (NMR):

LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl)
Small LDL 1811 nmol/l
Large HDL 0.0 mg/dl


In other words, small LDL constitutes 81% of all LDL particles (1811/2231), a severe pattern. Large HDL is the healthy, protective fraction and Kevin has none. These are high-risk patterns for heart disease. These, too, are patterns of carbohydrate intolerance.

Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance.

We could also cast all three conditions under the umbrella of "insulin resistance." But I prefer Carbohydrate Intolerance Syndrome, or CIS, since it immediately suggests the basic underlying cause: eating carbohydrates, especially those that trigger rapid and substantial surges in blood sugar.

CIS is the Disease of the Century, judging by the figures (both numbers and humans) we are seeing. It will dominate healthcare in its various forms for many years to come.

The first treatment for the Carbohydrate Intolerance Syndrome? Some would say the TZD class of drugs like Avandia. Others would say a DASH or TLC (American Heart Association) diet. How about liposuction, twice-daily Byetta injections, or even the emerging class of drugs to manipulate leptin and adiponectin? How do "heart healthy" foods like Cheerios and Cocoa Puffs fit into this? (Don't believe me? The American Heart Association says they're heart healthy!)

The first treatment for the Carbohydrate Intolerance Syndrome is elimination of carbohydrates, except those that come from raw nuts and seeds, vegetables, occasional real fruit (not those green fake grapes), wine, and dark chocolates.

Making sense out of lipid changes

Maggie had been doing well on her program, enjoying favorable lipids near our 60-60-60 targets (HDL 60 mg/dl or greater, LDL 60 mg/dl or less, triglycerides 60 mg/dl or less). Last fall, her last set of values were:

Total cholesterol: 149 mg/dl
LDL cholesterol: 67 mg/dl
HDL cholesterol: 73 mg/dl
Triglycerides: 43 mg/dl

The holidays, as with most people, involved a frenzy of indulgent eating: Christmas cookies, cakes, pies, stuffing, potatoes, candies, etc.

Maggie returned to the office 6 pounds heavier with these values:

Total cholesterol: 210 mg/dl
LDL cholesterol: 124 mg/dl
HDL cholesterol: 57 mg/dl
Triglycerides: 144 mg/dl

In other words, holiday indulgences caused an increase in LDL cholesterol, a reduction in HDL, an increase in triglycerides, an increase in total cholesterol.

What happened?

At first glance, many of my colleagues would interpret this as fat indulgence and/or a "need" for statin drug therapy.

Having done thousands of lipoprotein panels, I can tell you that, beneath the surface, the following has occurred:

--Overindulgence in carbohydrates from the goodies triggered triglyceride (actually VLDL) formation in the liver, released into the blood.
--Increased triglycerides and VLDL triggered a boom in conversion of large LDL to small LDL (since triglycerides are required to form small LDL particles) via cholesteryl-ester transfer protein (CETP) activity.
--Increased triglycerides and VLDL interacted with HDL particles, causing "remodeling" of HDL particles to the less desirable, less protective small particles, which do not persist as long in the blood, resulting in a reduction of HDL.

The critical factor is carbohydrate intake. This triggered a domino effect that is often misintepreted as excessive fat intake or a genetic predisposition. It is nothing of the kind.

I discussed this phenomenon with Maggie. She now knows to not overindulge in the holiday snacks in future and will revert promptly back to her 60-60-60 values.

How to Give Yourself Hashimoto's Thyroiditis: 101

I borrowed this from the enormously clever Dr. BG at The Animal Pharm Blog.


How to Give Yourself Hashimoto's Thyroiditis: 101

--lack of sunlight/vitamin D/indoor habitation
--mental stress
--more mental stress
--sleep deprivation... (excessive mochas/lattes at Berkeley cafes)
--excessive 'social' calendar
--inherent family history of autoimmune disorders (who doesn't??)
--wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?)
--lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc
--lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case)
--weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)



If you haven't done so already, take a look at Animal Pharm you will get a real kick out of Dr. BG's quick-witted take on things.


We are systematically looking for low thyroid (hypothyroidism) in everyone and findings oodles of it, far more than I ever expected.

Much of the low thyroid phenomena is due to active or previous Hashimoto's thyroiditis, the inflammatory process that exerts destructive effects on the delicate thyroid gland. It is presently unclear how much is due to iodine deficiency in this area, though iodine supplementation by itself (i.e., without thyroid hormone replacement) has not been yielding improved thyroid measures.

I find this bothersome: Is low thyroid function the consequence of direct thyroid toxins (flame retardants like polybrominated diphenyl ethers, pesticide residues in vegetables and fruits, bisphenol A from polycarbonate plastics) or indirect toxins such as wheat via an autoimmune process (similar to that seen in celiac disease)?

I don't know, but we've got to deal with the thyroid-destructive aftermath: Look for thyroid dysfunction, even in those without symptoms, and correct it. This has become a basic tenet of the Track Your Plaque approach for intensive reduction of coronary risk.

Framing

Heart health without a 12" incision



Heart health for less than $44,483 (Cost of a coronary stent according to the American Heart Association 2008 Update)



Track Your Plaque: A drug-free zone



Why an RDA for vitamin D?

The Food and Nutrition Board (FNB) of the Institute of Medicine is charged with setting the values for the Recommended Daily Allowances of various essential nutrients. However, when it comes to vitamin D, the FNB decided that "evidence is insufficient to develop an RDA and [an Adequate Intake, AI] is set at a level assumed to ensure nutritional adequacy."

The National Institutes of Health Office of Dietary Supplements lists the AI's for various groups of people:

14-18 years
Male 200 IU
Female 200 IU

19-50 years
Male 200 IU
Female 200 IU

51-70 years
Male 400 IU
Female 400 IU

71+ years
Male 600 IU
Female 600 IU


A reconsideration is apparently being planned in near-future that will (hopefully) incorporate the newest clinical data on vitamin D.

My question: Who cares what the FNB decides? Let me explain.

I monitor blood levels of 25-hydroxy vitamin D to assess the 1) starting level of vitamin D without supplementation, and 2) levels while on supplementation, preferably every 6 months (during sunny weather, during cold weather). I have done for the past 3 years in over 1000 people.

The requirement for vitamin D dose in adults, in my experience, ranges from as low as 1000 units per day to as high as 20,000 units per day, rarely more. The vast majority of women require 5000 units per day, males 6000 units per day to maintain a blood level in the desirable range. (I aim for 60-70 ng/ml.) A graph of the distribution of vitamin D needs in my area (Milwaukee, Wisconsin) is a bell curve, a curve more heavily weighted towards the upper vitamin D dose range.

Need for vitamin D to achieve the same blood level is influenced by age, sex, body size, race, presence or absence of a gallbladder, as well as other factors. But needs vary, even among similar people. For instance, a 50-year old woman weighing 140 lbs might need 4000 units per day to achieve a blood level of 25-hydroxy vitamin D of 65 ng/ml. Another 50-year old woman weighing 140 lbs might need 8000 units to achieve the same level, and 4000 units might increase her level to only 38 ng/ml. Two similar women, very different vitamin D needs. The differences can be striking.

Being a hormone--not a vitamin, as it was incorrectly labeled--vitamin D needs to be tightly regulated. We should have neither too little nor too much. I would liken it to thyroid hormones, which need to be tightly regulated for ideal health.

Now the FNB, in light of new data, wants to set new AI's, or even RDA's, for vitamin D for the U.S. This is an impossible--impossible--task. There is no way a broad policy can be crafted that serves everyone. It is impossible to state that all men or women, categorized by age, require X units vitamin D. This is pure folly and it is misleading.

The only rational answer for the FNB to provide is to declare that:

It is not possible to establish the precise need for vitamin D in a specific individual because of the multiplicity of factors, only some of which are known, that determine vitamin D needs. Individual need can only be determined by assessing the blood level of 25-hydroxy vitamin D prior to initiation of replacement and periodically following replacement to assess the adequacy of replacement dose. Continuing reassessment is recommended (e.g., every 6-12 months), as needs change with weight, lifestyle, and age.

Sure, it adds around $100-150 per year per person for lab testing to assess vitamin D levels. But the health gains made--reduced fractures, reduced incidence of diabetes, reduced colon, breast, and prostate cancer, less depression, reduced heart attack and heart procedures--will more than compensate.

Bargains for Armour Thyroid

We use Armour thyroid almost exclusively. I take it myself.

I am thoroughly convinced that, for at least 70% of people requiring thyroid replacement, the added T3 component makes a world of difference compared to isolated T4: More energy, greater alertness, better mental clarity, better weight loss, larger effects on lipoprotein(a).

However, there are substantial price disparities in different pharmacies.

For instance, in Milwaukee, a one month supply of 1 grain (60 mg) tablets costs:

Walgreen's: $36.00

Walmart: $9.54


That's a considerable price difference of nearly 400%. It therefore always pays to do a little bit of shopping.

Heart scan mis-information on WebMD

If you want information on how prescription drugs fit into your life, then go to WebMD.

But, if you are looking for information that cuts through the bullcrap, is untainted by the heavy-handed tactics of the drug industry, or doesn't support the "a heart catheterization for everyone" mentality, then don't go there.

A Heart Scan Blog reader turned up this gem on the WebMD site:

Should I have a coronary calcium scan to check for heart disease?

In their report, they list some reasons why a heart scan should not be obtained:

Most of the time, a physical exam and other tests can give your doctor enough information about your risk for heart disease.

You've got to be kidding me. What tests are they talking about?

EKG? An EKG is a crude test that tells us virtually nothing about the coronary arteries or risk for heart attack. It is helpful for heart rhythm disorders and other abnormalities, but virtually useless for coronary disease unless a heart attack is underway or has already occurred.

Cholesterol? What level of cholesterol tells you whether you have heart disease? Tim Russert, for instance, had the same cholesterol values 5 years before his death as on the day of his death. How would cholesterol have told his doctor that heart disease was present? Does an LDL cholesterol of 180 mg/dl tell you that someone has heart disease, while a value of 130 mg/dl does not?

Stress test? You mean like the normal stress test Bill Clinton had 3 months before his near-fatal collapse? Stress tests are a gauge of coronary flow, not of coronary atherosclerosis. Huge amounts of coronary plaque can be present while a stress test--flow--remains normal.

No, a physical exam does not uncover hidden heart disease. The annual physical is, in fact, a miserable failure for detection of hidden heart disease.


You already know that your risk for heart disease is low or high. The test works best in people who are at medium risk but have no symptoms.

This bit of fiction comes from a compromise statement in the American College of Cardiology and American Heart Association "consensus" document detailing the role of heart scans in heart disease detection. Because conventional thinkers don't like the idea of very early detection in seemingly "low risk" people, nor do they like the idea of diabetics and smokers getting a heart scan because it's "obvious" that they are already at high risk, the middle ground was taken: Scan only people at "intermediate risk."

What the heck is "intermediate risk"? Are you intermediate risk?

In real life, using standard criteria (e.g., Framingham scoring) to decide who is low-, intermediate-, or high-risk fails to identify over 1/3 of people with heart disease, while subjecting many without heart disease (plaque) to needless treatment (meaning statins, since that's the only real preventive treatment on most doc's armamentarium).

Another fact: Heart scans are quantitative, not just normal or abnormal. Your heart scan score could be 5, it could be 150, it could be 500, or 5000---it makes a world of difference. The risk of someone with a score of 5000 is at very different risk than someone with a score of 5. It also provides much greater precision in determining a specific individual's risk.



The test could give a high score even if your arteries aren't blocked. This might lead to extra tests that you don't need.

This is true--if you doctor has no idea what he's doing.

This is like saying that you should never take your car to the repair shop because all mechanics are crooks. If you have an unscrupulous cardiologist who tells you that your heart scan score of 25 means you are a "walking time bomb" and heart catheterization is necessary to determine whether you "need" a stent . . . well, this is no different than the shady mechanic who advises you that your car's engine needs to be rebuilt for $3000, when all you really needed was a few new spark plugs.

Coronary plaque is coronary plaque, and all coronary plaque has potential for rupture (heart attack)--even if it doesn't block flow. This is true at a score of 10, or 100, or 1000--all plaque is potentially rupture-prone, though the more plaque you have, the greater the likelihood.


Not all blocked arteries have calcium. So you could get a low calcium score and still be at risk.

They're missing the point: ANY calcium score carries risk, so a low score should not be interpreted as having no risk. But, just because a procedure like stenting or bypass surgery is not necessary to restore flow, it does not mean that risk for plaque rupture is not present--it is.

Any heart scan score should be taken seriously, meaning sufficient reason to engage in a program of heart disease prevention.

Although not perfect, coronary calcium scoring remains the easiest, most accessible, and least expensive means for identifying and quantifying coronary atherosclerosis--whether or not WebMD and drug industry money endorse them.

Heart disease prevention for the helpless, ignorant, or non-compliant

The media outlets are gushing with the "research"/marketing spinoff of the JUPITER trial, an analysis conducted by Dr. Erica Spatz of Yale University, that suggests that statin use should be expanded to many millions more Americans.

USA Today: Study: 11M more should get statins

MedPage: JUPITER Findings Could Boost Statin Use by 20%

Health Day: Millions More Americans Might Be Placed on Statins

WebMD: More May Benefit From Cholesterol Drugs: Study Shows More Would Qualify for Statin Treatment if Levels of C-Reactive Protein Are Considered


You may recall that the JUPITER trial (discussed previously in a Heart Scan Blog post) studied the cardiovascular event risk in people with "normal" LDL cholesterols (calculated, of course, not measured) of 130 mg/dl or less, along with increased c-reactive protein, a crude inflammatory measure, of 2.0 mg/dl or greater. A 54% (relative) reduction in cardiovascular events occured in the group taking Crestor 20 mg per day.

What I see is a confluence of events that have brought us to the "statin drugs are necessary for everybody" mentality:

--The low-fat diet advice of the last 40 years has increased non-fat or low-fat foods that increase LDL, since removing fat from the diet provokes small LDL particle production and increases the inflammatory measure, c-reactive protein (CRP).

--The proliferation of "healthy whole grains" in the diet have also caused an enormous boom in small LDL particles, which is interpreted to the uninformed as "high cholesterol." It has also provoked CRP substantially.

--The advice to reduce salt intake has brought a broad re-emergence of iodine deficiency. When thyroid hormone production flags due to lack of iodine, LDL cholesterol (both large and small) increase.

--Our lives, which are increasingly conducted indoors, have worsened the already substantial vitamin D deficiency. While deficiency of vitamin D primarily reduces HDL cholesterol and increases triglycerides, it can also cause an increase in small LDL and a large increase in CRP.


In other words, a collection of events have converged to provide the appearance of high LDL cholesterol and high CRP. This creates the appearance of a "need" for statin drugs. The JUPITER trial now exploits both the LDL-reducing and CRP-decreasing effects of statins.

I view the foisting of Crestor via the JUPITER argument on the public as taking full advantage of the helpless situation many Americans find themselves in: Reduce fat intake, eat more healthy whole grains and . . . cholesterol and CRP skyrocket! "You need Crestor! See, I told you it was genetic," says the doctor after attending the nice AstraZeneca-sponsored drug dinner.

The notion of using a drug like Crestor to suppress inflammatory patterns is absurd. There are far better, easier, cheaper ways to achieve this goal, along with dramatic reduction in cardiovascular risk. But, to the ignorant, the helpless, or non-compliant with real change in diet and lifestyle, then Crestor does serve a purpose.

I can only hope that the excessive pushing of statin drugs on the public will sooner or later trigger a revolt.

Dangerous mis-information on vitamin D


Please be aware of the ignorant propagating information they have no business talking about.

This is one such example, a newsletter from pop exercise guru, Denise Austin.

Although I'm sure she means well, I have a problem with people who have little to no experience acting as experts, often simply repeating something they heard or read somewhere else. This has become particular problem with the internet, in which bad information can get repeated thousands of times, gaining a veil of "truth" through its repetition. I don't mean to pick specifically on Ms. Austin, since she joins a growing rank of pseudo-experts on vitamin D and other topics, but she provides a good example of how far wrong mainstream information can be.



Simple Steps
Do Your D!


Calcium often gets all the glory when it comes to bone health. But calcium wouldn't benefit your bones much without its partner, vitamin D!

Why? Vitamin D helps your body absorb calcium and keeps your bones strong; without enough vitamin D, the bones become weak and brittle, a condition called rickets in children, and osteomalacia in adults. Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

Unfortunately, not too many foods contain vitamin D naturally. (Tuna and sardines canned in oil are exceptions.) The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals. You can check the Nutrition Facts panel on packages and containers to see which products contain vitamin D. It should be listed after vitamins A and C, along with the percentage of the Daily Value that a serving of the food contains. The Daily Value (a standardized amount) for vitamin D is 400 IU, so if your milk has 25 percent of the Daily Value, it provides 100 IU per serving.

Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week to make enough. However, because of the increasing incidence of skin cancer in recent years, many experts are wary about recommending sun exposure.

So take a closer look at milk, yogurt, cereal, and margarine selections when you're doing your weekly shopping, and stock up on brands that are fortified with vitamin D. Challenge yourself to consume one source of vitamin D at least three days in the coming week! If you cannot eat or do not like any foods that contain vitamin D or are fortified with it, talk with your health care provider ASAP about taking a supplement. Your bones will thank you for it!



Let me list the mistakes in this piece:

Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

This is the same non-information that was the advice originally offered by the Food and Nutrition Board based on a best guesstimate due to lack of data. It is clear from newer data that doses required for full restoration of vitamin D are in the thousands of units. (My personal dose for full restoration of vitamin judged by serum levels of 25-hydroxy vitamin D is 8000 units per day.)

The information coming from the Food and Nutrition Board is about as good as the information coming from the USDA (you know, that "government" agency meant to represent the interests of ConAgra, Cargill, and Big Farming) and the American Heart Association (that represents consensus opinion from data 20 years out of date and now arm-in-arm with Big Food like General Mills, Kraft, and Nabisco). These agencies and the advice they offer has, over the past few years, become increasingly irrelevant and outdated. It is the Information Age, in which ulterior motives are becoming more readily exposed, yet they still operate by the rules of the Industrial Age and deliver a message that serves their own purposes.

Ms. Austin fell for it.


The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals.

First of all, what is a "diet expert" doing advocating industrial foods? Cereals, in particular, are among the worst foods on the supermarket shelves, whether or not they are fortified. Candy bars can be fortified, too; that doesn't make them any better for you.

The vitamin D added to these foods is, more often than not, the ergocalcferol, or D2, form that is woefully ineffective. And the dose added is trivial, usually in the 100-200 unit range per serving. The same goes for the milk, an inadequate source that we don't even factor into total intakes because of the low quantity.


Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week.


Nope. This might be true for a young person below age 30 in a southern environment. It is NOT true for the majority of people in northern climates and anyone over age 30 or 40, since we lose most of the capacity to activate vitamin D in the skin as we age. A deep, dark Florida tan does not necessarily mean that vitamin D has been activated. See A tan does not equal vitamin D. Here in Wisconsin, where, despite this darn cold winter, does enjoy wonderfully warm and beautiful summers, the average vitamin D dose need ranges from 4000-8000 units per day in summer, slightly more in winter.

By the way, it is not calcium that is instrumental to bone health. It is vitamin D. Calcium is the passive bricks and mortar of bones, while vitamin D is the bricklayer, the determinant of calcium's fate, the master control of bone health. Calcium supplementation becomes almost immaterial when vitamin D is restored.

I praise Ms. Austin for her hard work, trying to help fat Americans lose weight. But please ignore her advice on vitamin D, along with the numbing repetition of this mis-information that will likely propagate from other exercise gurus, dietitians, and pseudoexperts.

A Tale of Two LDL's

Kurt, a 50-year old businessman with a heart scan score of 323, had a :

--Conventional (calculated) LDL of 128 mg/dl
--Real measured LDL 241 mg/dl.


Laurie, a 53-year old woman who underwent a coronary bypass operation last year (before I met her), had a:

--Conventional LDL of 142 mg/dl
--Real measured LDL was 85 mg/dl.


(By "real, measured" LDL, I'm referring to LDL particle number in units of nmol/L obtained through NMR lipoprotein testing and dividing by 10, or just dropping the last digit to convert the value to mg/dl. This technique was arrived at by comparing the population distributions of these two parameters, LDL particle number and calculated LDL. This is the gold standard in my view. Similar numbers can be obtained by measuring apoprotein B, direct LDL, or calculated non-HDL, with diminishing reliability from first to last.)

In other words, Kurt's conventional LDL underestimated real LDL by 88%. Laurie's conventional LDL overestimated real LDL by 40%.

Interestingly, Laurie's doctor had insisted she take Lipitor for a high LDL cholesterol. Her real LDL was, in fact, low to begin with and benefits of a statin drug would be little to none. (Remember, in our Track Your Plaque approach, multiple other treatments are included, such as omega-3 fatty acids from fish oil, vitamin D normalization, and wheat elimination, strategies that yield benefits that others expect to obtain with statins.) Laurie's real cause of her heart disease proved to have nothing to do with LDL cholesterol, but involved lipoprotein(a) and thyroid issues.

Kurt proved to have a severe preponderance of small LDL particles--the worst kind of LDL, while Laurie had none--a benign pattern.

Then how can anyone make sense of the conventional, calculated LDL cholesterol that is generally (95% of the time) provided? If accuracy can stretch to plus or minus 80% . . . you can't. Conventional LDL is a miserably inaccurate number. The problem is that obtaining a superior number requires a step or two more testing and insight, something most busy primary care doc's simply don't have in the midst of a day filled with arthritis, bronchitis, diarrhea, belly aches, and seborrhea.

Yet conventional--I call it "fictitious"--LDL serves as the basis for this $27 billion (annual revenues) industry selling statin drugs.

This is meant to be neither an argument in favor of nor against statin drugs. However, it is plain as day that any study designed to reduce LDL cholesterol will be hopelessly clouded by calculated LDL imprecision. A calculated LDL of, say, 143 mg/dl might really be 187 mg/dl, or it might be 74 mg/dl--you can't tell by looking just at LDL. Yet billions of dollars of research and billions of dollars of healthcare costs are based on the treatment of this number.

This reminds me of the mark-to-market accounting magic that helped topple Wall Street.

I don't think that the statin world is poised for such a huge downfall. But I do see this as a source of enormous dilution of the effects of statin drugs. People who barely stand to benefit get the drugs, while others who might truly benefit are treated inadequately. It provides fuel to the growing idea that reducing LDL cholesterol fails to truly provide benefit.

I am no lover of statin drugs nor drugs in general. But I am a fan of knowing the truth. Despite my bashing of the drug industry (and make no mistake: the drug industry is a cutthroat, profit-seeking, do-anything-to-increase-sales industry), I do believe that there is a role for statin drugs (though far smaller than $27 billion per year). But the usual method of selecting people for treatment is pure fiction. The ATP-III cholesterol treatment guidelines? An anemic attempt to apply structure to meaningless values.

You and I do not need to subscribe to this sort of non-quantitative nonsense.