Since vitamin D has been the topic of a fair amount of media coverage, I've received many questions about this fascinating "nutrient." A day doesn't go by without several nurses, friends, even fellow physicians stopping me to ask about vitamin D.

When I inform them that the average dose for females in this region (upper Midwest) is 4000-5000 units per day, 5000-6000 units per day for males, they are all surprised. "Then why did they say just take your multivitamin every day, or just drink your milk on the news?"

Many people are even more surprised, sometimes completely turned off, when they hear that, to be truly confident of adequate vitamin D dosing, a blood level of 25(OH) vitamin D3 needs to be checked. Now we're talking real hassle!

But there is no other way to do it. In order to obtain the full potential benefits of vitamin D, such as reduction in blood sugar and sensitization to insulin, reduction in cancer risk (especially prostate, colon, and breast), reductions in blood pressure, increased bone density, not to mention markedly increasing the likelihood of stopping or reducing your heart scan score, then achieving a desirable blood level of 25(OH) vitamin D is necessary.

Checking a blood level of vitamin D is no more difficult than having a cholesterol test, unless, of course, your doctor balks at the idea. (Time for a new doctor if that occurs.)

All too often, someone will be convinced they are taking a sufficient dose of vitamin D of, say 2000 units per day, only to discover that their blood level of 25(OH) vitamin D is something like 17 ng/ml--severe deficiency, sufficient to leave them exposed to all the undesirable consequences of vitamin D deficiency. Even though 2000 units per day represents 500% of the Institute of Medicine's recommended Adequate Intake for adults, to those familiar with the Track Your Plaque program it likely sounds like a child's dose.

Many variables enter into the equation in your body that determines your need for vitamin D: body size (heavier or larger people need more, with obese people often requiring enormous doses); sex (men need more than women); age (aging results in dramatic loss of ability to activate vitamin D in the skin); race; skin color (darker skinned people require more). Trying to guess your need is a fool's game. It's also a game that can seriously compromise your health and your hopes of ever stopping or reducing your heart scan score.

The message is clear: You cannot guess what your vitamin D need is. You cannot properly judge your vitamin D requirement by your age, body size, sex, or any other characteristic. Having a tan or a lack of a tan is a lousy indicator, as well. A simple blood level of 25(OH) vitamin D is an absolute necessity to gauge your vitamin D status, both before starting and while on your supplement.

Members of Track Your Plaque: Watch for the 30-some page booklet, The Track Your Plaque Complete Handbook on Vitamin D and Heart Health, which will be released in the next day or two.

Copyright 2008 William Davis, MD

According to the poll just completed by 80 participants on The Heart Scan Blog, 50% of respondents said they were less likely to take a drug after viewing an advertisement for it. A whopping 3 (4%) said that they would be more likely to take the drug after viewing an advertisement.

I find that interesting. If half the people responding are less likely to become customers of a drug company, then how does the drug industry justify running around-the-clock, every-few-minute ads? Spending by the drug industry for direct-to-consumer (DTC) advertising has ballooned over the past few years, and is now well over $30 billion dollars per year.

Unfortunately, despite the views of the highly-educated, curious, think-for-yourself, health information-seeking sorts of people who read this blog, drug companies still come out on top by DTC advertising. Estimates vary, with a 2006 U.S. Government Accountability Office study reporting that, for every $1 DTC advertising, sales are increased by $2.20. A 2000 Harvard study showed a higher return of $4.40 for every advertising dollar spent.

I'm sure the drug companies themselves have a very tight accounting handle on their own set of figures. We may not be terribly fond of these people and their often suspect tactics, but they're not stupid. They are certainly not stupid when it comes to making money.

Interestingly, 80% of the funds spent on DTC advertising focus on the 20 or so most popular drugs, all of which are used for treatment of chronic conditions like high cholesterol and high blood pressure, markets that are large and long-term. It pays very little to advertise drugs that may serve small markets for a short period. The implicit message is that this is not at all about informing the public. It is about advertising to grow revenues and profits--pure and simple.

It makes me wonder what the results of our poll would have been had we conducted it in 2000 before many people hadn't yet been brought to the brink of vomiting from the endless onslaught of commercial after commercial, complete with smarmy spokespeople (a la Lipitor's Dr. Robert Jarvik). What will it show in two years? Will the broader public join the more informed people who read this blog and become increasingly inured to the hard sell tactics?

For further discussion of this topic, click here for a reprint of an August, 2007 New England Journal of Medicine study, A Decade of Direct-to-Consumer Advertising of Prescription Drugs provides background, along with commentary on the impact of DTC drug marketing since the FDA allowed it 10 years ago. (Because it is a study and not an editorial, the editors fall short of making any recommendations for improvement or calling for a moratorium.)

Copyright 2008 William Davis, MD

Anna responded to the Heart Scan Blog post, Can you say "sugar"? with the following wonderfully telling comment:

A measured bowl of Cheerios and a bit of milk (whole, because it's what I had), equal to 75 grams of carbohydrate, gave me the highest ever blood glucose reading from a food (not counting glucose solution from a Glucose Tolerance Test). I was attempting a "homemade" version of a 3 hr GTT before going to my doctor with my concerns about my BG.

My BG started to rise very fast within 15 minutes after eating the cereal, peaked at about 250 mg/dL at 45 minutes, then slowly dropped. By about 60-75 minutes, I experienced strong hunger and carb cravings as the BG began to slowly drop, and by about 2.5 hours after eating, my BG had suddenly dropped quite low (in the low 70s) and I had developed a nasty hypoglycemic feeling (shaky, irritable, craving sugary foods, headache, etc.).

It's hard for me to see "heart healthy" Cheerios (or any other highly processed breakfast cereal) as anything other than a bowl of pre-digested sugar that contributes to roller coaster blood glucose and insulin levels, which a great way to start anyone's day. Certainly, I don't do well with Cheerios because I clearly have a damaged glucose regulatory system (probably a diminished or absent first phase insulin response, but I can't imagine that it is doing any good for people with healthy glucose regulation, either.

I banned prepared cold cereals from our house. If my 9 yr old son gets cereal at all at home, it's whole groats (not even rolled or steel cut because those aren't truly "whole grain" anymore), soaked overnight in some water and a tsp of plain yogurt (soaking neutralizes phytates and reduces cooking time), then cooked about 8-10 minutes (water added as necessary). Sometimes I add a bit of quinoa or almond meal prior to soaking to boost the protein content a bit. I garnish with a pat of butter, some heavy cream, and a dusting of cinnamon. If I'm feeling *really* indulgent, I drizzle about 1 tsp of Grade B maple syrup on top (Grade B is stronger in flavor and so less can be used). I don't eat this cereal myself, and truthfully, I'd rather my son not, either, but he sometimes wants cereal. It's the least damaging compromise I can come up with that we can both live with.

I have also seen diabetic effects from Cheerios: rises in blood sugar, exagerration of small LDL, drops in HDL, rises in triglycerides. Yes, it may reduce LDL a small quantity, but so what?

The Cheerios "heart healthy" claim is based on a piece of research apparently performed by Dr. Donald Hunninghake at the University of Minnesota and reported in 1998:

A study conducted at the University of Minnesota Heart Disease Prevention Clinic and published as "Cholesterol-Lowering Benefits of a Whole Grain Oat Ready-to-Eat Cereal" in the May issue of the Nutrition in Clinical Care journal in 1998, showed that people can lower their blood cholesterol by an average of 3.8% over six weeks by enjoying 3 cups of cold cereal made with 100% whole grain oats everyday as part of the meals and snacks in a healthy lower-fat diet.

(Unfortunately, I could not locate the actual publication. It doesn't mean it doesn't exist; I just couldn't locate it. Perhaps it's in a small journal not entered into the online publication database.)

The purported effects of Cheerios should not be confused with that of actual, intact oat bran, as suggested by studies such as those of Brenda Davy et al, High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men, in which significant reductions in LDL particle number and small LDL (NMR) were obtained. (This study was also supported by Quaker Oats.) Several studies have shown that oat bran does indeed reduce LDL cholesterol, sometimes as much as 30-50 mg/dl. Cheerios can not even come close to this.

If Cheerios were nothing more than finely pulverized oats, then perhaps it wouldn't be so bad. But add corn starch and sugar, and you have ingredients that have potential to distort LDL particle size and yield blood sugar-escalating effects like those described by Anna.

The gravity of perpetuating these myths is brought home by a testimonial posted on the website for Cheerios:

“I had unexpected open heart surgery a year ago. As I adopted heart health habits during my recovery, I realized that I should have been eating the Cheerios cereal I carried around in a plastic baggie so many years for my kids!”

Beverly
Scotch Plains, NJ

It makes me shudder.

Copyright 2008 William Davis, MD

There's a wonderful blog called The IF Life: Intermittent Fasting and Instant Freedom. It is written by personal trainer (and apparently former corporate bigshot), Mike O'Donnell.

Mike has a great take on brief, intermittent fasting that I found helpful and I believe you will also.

Intermitent Fasting 101: How to Start, Part I

The biggest question people have is how to effectively use IF (intermittent fasting) to achieve their goals and maximum results. These results and goals can vary by each person with fat loss, muscle gain, better health, improved performance in your sport of choice and more. With that comes the individuality of what is a person’s insulin resistance, current body composition (bodyfat%), daily lifestyle, eating habits, macronutrient ratios (carbs/protein/fat), type of exercise program, frequency and volume of training, recovery demands, and so forth. You are unlikely to find 2 people with the same set of parameters and same exact responses to an IF protocol. What does this mean? Well just that we need to start with a basic IF program, and then learn how to monitor results and adjust as we go. Even down the road things will change as you will improve health, lower insulin resistance and maybe change performance and recovery needs. So nothing is ever just one set way. Life is dynamic (always changing and evolving) and so should be the way we see our own journey for health and fitness.

What is IF?

For those that may not be familiar to the term, intermittent fasting is just taking times of fast (no food) and working them into your lifestyle. This can be either daily or a couple times a week (will get into that more below). Benefits include improving insulin resistance (which you will hear alot about as being the #1 key marker in so many health factors including weight loss, muscle gain, performance, recovery, anti-ageing and disease prevention) and giving the body a chance to do some internal cleaning (or housework), which can lead to improved immune function and overall health. If you want to see studies of all the benefits of IF/CR, please the resources page.

How do I begin to IF?

Is there only one set way in which to do IF? No. I could easily come up with 10 different IF protocols based on 10 people’s individual’s needs, lifestyle, exercise, goal, macronutrient ratios, and so forth. We will keep it simple and give the 2 most frequent and basic options.

Daily Fasting: Typically done every day and only giving the person a smaller eating window in which to get their calories. (for example, a 18hr daily fast would mean someone would only eat every day between the hours of Noon and 6pm). You will see varying times from 15-19 hours for daily fasting.
Fasting 1-3x a week: This could also be called alternate day fasting/calorie restriction (for those doing it every other day). This is just fasting of usually longer periods 18-24 hours but only 1-3x a week. Many variations to play with here.
“But which one is better and how to I do it now if I want…….”. Whoa, slow down. I know many have questions but let’s still try to keep this simple for now and expand into more specifics later. So far many people have experimented with both types of IF and have seen great results. But you also have to take into account all the other variables such as what is the person eating in that window? Is is junk food? Is it low carb? How many times a week are they doing it? Are they overweight and wanting just fat loss? Are they lower bodyfat but looking for improved performance and health? How many times a week are they exercising? What kind are they doing and what intensity? The list can go on and on, but let’s start to analyze the 2 types of IF and let you decide which one best suits your lifestyle.

Daily Fasting (15-19 hours):

The Advantages are:

--simple eating strategies for every day
--even people that may not eat 100% clean foods can see weight loss due to the smaller window and lower calorie total per day

The Disadvantages are:

--Can possibly lower metabolism if calories are too low for too long (not what you want if your #1 goal is weight loss)
--Not getting enough food in the smaller window may also lead to muscle loss for more active people (not good)
Fasting 1-3x a week:

The advantages are:

--Allows a person to make sure they are getting enough calories on the non-fasting days, and then just keeps to a simple small feed window (if any) on the IF days.
--Simple thinking for people who do not have experience in how to eat clean to eat one day, and then eat in a smaller window the following day (alternate day fasting/CR). This can achieve fat loss for people who are mostly overweight and may not be too active. (of course don’t get me wrong, that eating healthy is our main goal but this can be a good step for some people to start their weight loss jounrey and learn how to make better choices as they go)

Disadvantages:

--Doesn’t force a person to make better choices with their food (as one could probably eat junk one day, and then fast the next and still lose weight). Not something we want long term because this is not going to improve your other health markers (diseases prevention, insulin resistance) like a good IF program on healthy foods.

Again I can’t say it enough, as there are so many variables to play with in an IF program. Some people may say “well it didn’t work for me” or “I didn’t gain any muscle”. Well unless I know everything about what you do for exercise daily, your total calories, when you eat and your macronutrient ratios (protein/carbs/fats), I can’t even begin to help. IF is a simple tool to start with, but you have to take full responsibility for your own health and progress and learn when it is not working and when to change things up! Like I said, if it is NOT working then stop IF and rethink your attack plan (or get a professional to coach you on it).

So to sum up, here are some examples of what you can play with:

Daily Fasting of 15-19 hours. I would highly suggest that if you do this make sure you are recovering from your exercise and start only Mon-Fri and give yourself the weekends to eat all day (hopefully with healthy choices of course)

Fast 1-2x a week to start if you have never done any fasting or do not know how to eat healthy and control your macronutrients. Start with 1-2 days a week with fasts of 18-20 hours (I wouldn’t start with 24 hr fasts to begin as most people can not handle the hunger cravings and in turn will just end up eating all the wrong foods when they do eat) and say eat only from say 1pm-6pm for example. Drink lots of water (add lemon, your liver will appreciate it! and it will help with the hunger). For example, fast Wed and Sun (or whatever days fit into your schedule)

Or you can do a mixed approach and fast every other day for a small eating window. For example eat all day Mon, only 12-6pm on Tues, all day Wed, 12-6pm on Thurs, etc. Start with bigger eating windows and make them smaller as you get used to fasting. This approach may work for people who have alot of weight to lose and can not (I should really say “will not” as everything is a choice!) eat 100% healthy for the moment. This approach may not work for more advanced people who have a high activity level unless you are getting a ton of health calories in that fasting window.
“So What Do I Eat on the Fasting Days?”

That’s the best part, you should be able to eat unlimited healthy foods (healthy proteins, fats, veggies, fruit, nuts…see Paleo Diet in the resources page). If you are eating more processed foods, breads and other high calorie intakes then you may have to monitor and control portions. Please know this is NOT about chronic calorie restriction or starving yourself. When I do weeks of eating 1-7pm, I am eating a ton of protein and veggies (complex carbs pwo also). I am hardly starving myself. I am not taking in 4000 cal a day however, so my daily average of say 2200-2500 cal is still low compared to the alternative. If you want to lose weight of course you will need a calorie deficit to pull the “stored energy” out of fat cells. That is the advantage to eating “Paleo”, you can’t over eat on protein, healthy fats, fruits (in moderation) and veggies. If you are making bad choices or starving yourself on IF, you may lose the effectiveness or slow progress. All goes back to the fact that if it is not working, then change something up! (there is always something that can be changed…and food choices is the #1 place to start!) I don’t count calories, and by eating natural foods that have been around for 100s of years….I don’t need to! (eating healthy natural foods will not only help you lose weight but also improve your health and lower your risks of diseases….so eating for health should always be the #1 goal in any program)

Hopefully this will give a good overview while trying to keep it simple. Remember it’s your journey to take, measure progress and adjust things that are not working. Start with one approach, and modify it. Who knows, your approach may change every couple months and that is ok. Life is always changing and so should your approach to health and fitness (as the body always responds better to change than sticking with the same eating/exercise approach for a long period of time).

All of these products bear the American Heart Association Check Mark of approval emblem, signifying that they are "heart healthy":

Kellogg's Frosted Mini-Wheats cereal

Ingredients:WHOLE GRAIN WHEAT, SUGAR, STRAWBERRY FLAVORED CRUNCHLETS (SUGAR, CORN CEREAL, CORN SYRUP, MODIFIED CORN STARCH, PARTIALLY HYDROGENATED COTTONSEED AND/OR SOYBEAN OIL, CITRIC ACID, GLYCERIN, NATURAL AND ARTIFICIAL FLAVOR, RED #40, BLUE #2), NATURAL AND ARTIFICIAL STRAWBERRY AND CREME FLAVOR, SORBITOL, GELATIN, REDUCED IRON, NIACINAMIDE, ZINC OXIDE, RED #40, PYRIDOXINE HYDROCHLORIDE (VITAMIN B6), RIBOFLAVIN (VITAMIN B2), THIAMIN HYDROCHLORIDE (VITAMIN B1), FOLIC ACID, BLUE #1, AND VITAMIN B12. TO MAINTAIN QUALITY, BHT HAS BEEN ADDED TO THE PACKAGING.

Orville Redenbacher popcorns

Dora the Explorer Cereal

Cheerios

The following requirements must be met to gain approval of the Check Mark program:

1) total fat 3.0 grams or less per serving

2) saturated fat 1.0 gram or less per serving

3) 20 grams or less cholesterol per serving

4) 480 mg or less sodium per serving

5) "Jelly Bean Rule": 10% of the Daily Value of 6 nutrients (e.g., fiber, vitamins A and C, etc.) must also be contained in each serving.

Had the Check Mark program focused on genuine nutrition and rated products by:

1) Healthy oil content

2) Sugar content or sugar-equivalents, i.e., glycemic index or load

3) Impact on HDL, small LDL, triglycerides

none of these products would have made the list, not even close.

Gilbert is a 58-year old high school science teacher.

When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.

I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero also; it means less intensive efforts less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since the risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.

Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.

Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.

18 months later, Gil's 2nd heart scan score: 1410--a near doubling. Unsettling to Gil and to us, to say the least.

How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?

I fear that the culprit might be warfarin.

Warfarin, better known by its brand name, Coumadin, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.

It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:

--Accelerate aortic valve calcification
--Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
--Accelerate osteoporosis
--Induce an artificial situation of vitamins K1 and K2 deficiency.

The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are the above list of various pathologic calcifications.

I therefore wonder if warfarin dramatically accelerated the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.

That all said, I am quite certain it was the warfarin.

Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.--serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)

My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweight the risks--including that of possible accelerated calcification of multiple sites.

Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.

Caraballo PJ, Heit JA, Atkinson EJ et al. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med 1999; 159 (15): 1750–6. PMID 10448778.

Pilon D, Castilloux AM, Dorais M, LeLorier J. Oral anticoagulants and the risk of osteoporotic fractures among elderly. Pharmacoepidemiol Drug Saf 2004;13(5): 289–294.PMID 15133779.

Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF. Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med 2004; 166(2):241–246.PMID 16432096.

Copyright 2008 William Davis, MD

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies

Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.

Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.

Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.

From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).

In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:

Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?

Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect.

Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years.

Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL.

I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID.

The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases.

Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry.

Every once in a while, they are worth paying attention to.

The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.

Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.

Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:

The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:

The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.

Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

One ounce of raw almonds (about 23 nuts) contains:

6 grams protein

14 grams fat

6 grams carbohydrate

3.5 grams fiber

For a total of 163 calories per ounce.

(From the USDA Nutrient Database)

Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released.

The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency.

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds.

One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods.

Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release).

If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter.

If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally.

My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides.

Some other observations with almonds included:

The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds.

Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts).

Copyright 2008 William Davis, MD

What is C-reactive protein (CRP)?

It is a blood-borne protein that originates in the liver and serves as an index of the body's inflammatory state. It is triggered by yet another inflammatory signal molecule, interleukin-6.

What triggers this cascade of inflammatory markers? Any inflammatory stimulus, such as being overweight, lack of exercise, vitamin D deficiency, viral illness no matter how trivial, any inflammatory disease like arthritis, small LDL, high triglycerides, poor diet rich in processed foods, resistance to insulin, any injury, incipient diabetes, hidden cancer, lack of education (no kidding), etc.

In other words, many, many conditions, from trivial to serious, trigger increased inflammatory markers like CRP.

A recent analysis (Genetically elevated C-reactive protein and ischemic vascular disease of persons with genetically elevated levels of CRP) suggests that CRP does not, by itself, cause atherosclerotic disease. CRP is therefore simply a marker for conditions that heighten inflammatory responses.

The AstraZeneca people sponsored the enormous JUPITER study of the statin drug, Crestor, that has been causing a stir, mostly glowing pronouncements of how the world would be a better place if everyone took Crestor.

In JUPITER, nealry 18,000 people (men 50 years and over, women 60 years and over) took 20 mg per day Crestor for two years. Participants all had starting LDL cholesterols in the "normal" range of no higher than 130 mg/dl and elevated CRP of 2 mg/dl or greater.

Crestor treatment resulted in 44% reduction in nonfatal heart attack, nonfatal stroke, hospitalization for unstable angina, revascularization (bypass surgery, stents) and death from cardiovascular causes. The reduction in nonfatal heart attack was most marked at 55%.

Admittedly, these are impressive results. Benefits held true for both males and females. At the very least, JUPITER should put to rest some of the fringe arguments that statins do not reduce cardiovascular events. They do. There is no sense in arguing against that. While we might argue about the value of statins in various subsets of people, there is no doubt that they do indeed exert a significant effect.

However, contrary to the hype and broad pronouncements of my colleagues, my concerns are:

1) Rather than shotgun the inflammatory response with a statin drug regardless of cause, doesn't it make more sense to ask why a specific individual has an increased CRP in the first place? For instance, if the answer is vitamin D deficiency, doesn't correction of the deficiency make more sense? (Vitamin D by itself reduces CRP around 60%--more than statin drugs.) Not to mention you obtain all the extraordinary benefits of vitamin D restoration, such as reduced cancer risk, increased bone density, relief from winter "blues," rise in HDL, etc. How about junk foods, obesity, and unrelated inflammatory conditions? Would we therefore indirectly be treating obesity with Crestor?

2) Crestor 20 mg per day, contrary to the study and to many statin studies, will not be tolerated for long by the majority. Muscles aches are not common--they are inevitable, sometimes incapacitating. While JUPITER showed 15% of both treatment and placebo groups experienced muscle effects--no different--this is wildly contrary to real life.

3) While there was a 55% reduction in the number of heart attacks, there continued to be a substantial number of heart attacks in the Crestor treatment arm. Clearly, reduction of CRP with Crestor, while helpful, is not a cure.

I view studies like JUPITER as simply an interesting piece of semi-scientific evidence, tainted to an unknown degree by commercial interests (including those of Dr. Paul Ridker, one of the principal investigators). It is not a mandate to use Crestor carte blanche in people with elevations of CRP.

My interpretation of these data in a practical sense is that Crestor 20 mg per day as sole therapy is useful in a disinterested, non-compliant patient who is unwilling to make substantial changes in lifestyle and nutrition. Helpful? Yes, but hardly an invitation for the world to take Crestor.

I believe that doesn't include any of the readers of this blog.

It is now a rare person who does not have at least some proportion of their LDL cholesterol as small particles. I estimate that, of the people who come to the office or report their data on the Track Your Plaque website, 90% have at least 40-50% small LDL particles. Some people have 100% small LDL particles. The sample NMR lipoprotein report shows the result for someone with a severe small LDL pattern (the tallest red bar labeled 1354 nmol/L, compared to the 74 nmol/L of the tiny red bar of large LDL.)

The nutritional approach for small vs. large LDL differs. Small LDL particles are most sensitive to carbohydrate intake; large LDL particles are more sensitive to saturated fats.

The conventional "heart healthy" diet that restricts saturated fat reduces large LDL but exerts no effect on small LDL. Thus, a diet that is restricted in saturated fat and weighed more heavily with "healthy whole grains" triggers small LDL particles. Followers of the conversations here recognize that small LDL particles are flagrant triggers for coronary plaque; they have, in fact, become the number one most common cause for heart disease in the U.S.

When you have lipoproteins tested, you can therefore gauge the likely result obtained when specific dietary changes are made. Follow the low saturated fat advice, large LDL will drop modestly, but small LDL skyrockets.

(Image courtesy Liposcience, Inc.)

Eliminate sugars, wheat, and cornstarch and you will see small LDL plummet (along with total LDL).

As an aside, my personal observation is that the "need" for statin cholesterol drugs can be reduced dramatically by paying attention to this important LDL size distinction.

Twenty years ago, the American farming industry experienced a dilemma: How to grow more soybeans, corn, or wheat from a limited amount of farmland, raise more cattle and hogs in a shorter period of time, fatter and ready for slaughter within months rather than years?

(Image courtesy Wikipedia)

The solution: Synthetically fertilize farmland for greater crop yield; “factory farms” for livestock in which chickens or pigs are crammed into tiny cages that leave no room to turn, cattle packed tightly into manure-filled paddocks. As author Michael Pollan put it in his candid look at American health and eating, The Omnivore’s Dilemma:

“To visit a modern Concentrated Animal Feeding Operation (CAFO) is to enter a world that for all its technological sophistication is still designed on seventeenth-century Cartesian principles: Animals are treated as machines—“production units”—incapable of feeling pain. Since no thinking person can possibly believe this anymore, industrial animal agriculture depends on a suspension of disbelief on the part of the people who operate it and a willingness to avert one’s eyes on the part of everyone else. . .”

Pollan goes on to argue that the cultural distance inserted between the brutal factory farm existence of livestock and your dinner table permits this to continue:

“. . .the life of the pig has moved out of view; when’s the last time you saw a pig in person? Meat comes from the grocery store, where it is cut and packaged to look as little like parts of animals as possible. The disappearance of animals from our lives has opened a space in which there’s no reality check on the sentiment or the brutality . . .”

The same disconnect has occurred in healthcare for the heart. The emotional distance thrust between the hospital-employed primary care physician, the procedure-driven cardiologist, the crammed-into-a-niche electrophysiologist (heart rhythm specialist) or cardiothoracic surgeon whose principal concerns are procedures—with an eye always towards litigation risk—mimics factory farms that now litter the landscape of the Midwest. The hospitals and doctors who deliver the process see us less as human beings and more as the next profit opportunity.

The “factory hospital” has allowed the subjugation of humans into the service of procedural volume, all in the name of fattening revenues. Never mind that people are not (usually) killed outright but subjected to a succession of life-disrupting procedures over many years. But whether livestock in a factory farm or humans in a factory hospital, the net result to the people controlling the process is identical: increased profits.

The system doesn’t grow to meet market demand, but to grow profits. The myth that allows this growth is perpetuated by the participants who stand to gain from that growth.

See hospitals for what they are: businesses. Despite most hospitals retaining "Saint" in their name, there is no longer anything saintly or charitable about these commercial operations. They are ever bit as profit-seeking as GE, Enron, or Mobil.

This post carries on the line of conversation begun in The Origins of Heart Catheterization: Part I and Part II.

While Dr. Sones labored in the relative obscurity of his catheterization laboratory, the American public was experiencing a crisis in healthcare availability, particularly among the over-65 age group. The population of elderly in the U.S. was growing rapidly. Between 1950 and 1963, their ranks grew from 12 million to 17.5 million. The cost of hospital care was also increasing 6.7% annually, several times the rate of increase in the cost of living of the time. From 1950 to the day of Dr. Sones’ discovery, the average cost for a day in the hospital jumped from $29 to $40. As a result, private health insurance carriers were forced to increase rates, driving premiums higher and farther out of reach for many. Half of all elderly were uninsured. Many feared that, while the sophistication of medical services advanced, healthcare was becoming increasingly unavailable to many, perhaps most, Americans.

The pivotal contribution that ignited wide dissemination of healthcare technology didn’t come from a physician, nor someone in healthcare. It was spurred by a nearly-forgotten bureaucrat. Without the behind-the-scenes laboring of this one man, the present healthcare system might be quite different.

It was largely the work of Nelson H. Cruikshank, an ordained Methodist minister with a Master of Divinity degree and veteran of battling for rights of the elderly and poor deprived of health care. For 10 years, Cruikshank served as director of the AFL-CIO's Social Security Department and had been instrumental in getting the Social Security Disability act passed. Working on the side of organized labor but maintaining the public demeanor of a church pastor, Cruikshank gained a reputation as a fighter for the working man, one who didn’t back down from a political brawl. In an interview regarding the question of corporate-retained earnings for capital investment, he blasted the practice, calling it "taxation by corporation without representation. Through prices paid for consumer goods, buyers are providing capital for industries over which they have no control and from which they receive no dividends” (Time Magazine, Dec. 20, 1948).

For years, Cruikshank lobbied tirelessly on behalf of American unions to bring the new national healthcare bill, known as Medicare, to a vote on the floor of Congress. Numerous efforts at a national program had languished for a decade before Medicare was drafted, and the Medicare legislation remained bottlenecked for years in committees. Cruikshank’s relentless and forceful persuasion was instrumental in finally bringing the bill to a vote. Among the most vocal opponents Cruikshank parried was the American Medical Association (AMA), terrified that the new program would lead to loss of control over healthcare delivery and reimbursement. The AMA labeled Medicare "the most deadly challenge ever faced by the medical profession."

Cruikshank proved how tough he was when he faced off with Dr Morris Fishbein, then president of the AMA, in a radio debate. Oscar R. Ewing, attorney and Democratic political organizer under the Truman administration, offered these reminiscences of the debate:

“Dr. Fishbein described the horrible confusion that existed in the [government-run] British Health Service that had recently been established in Britain. He told of the utter confusion that he found existed when he was in England a few weeks previously; that there were long queues in every doctor's office, that doctors were overburdened with paper work; that a mother who wanted an extra allowance of milk for her sick child had to get a doctor's prescription for it and then go to the Healt All posts by william-davis

Disease Engineering

20. October 2008 William Davis (0)

Imagine you contract pneumonia.

You have a fever of 103, you’re coughing up thick, yellow sputum, breathing is getting difficult. You hobble to the doctor, who then fails to prescribe you antibiotics. You get some kind of explanation about unnecessary exposure to antibiotics to avoid creating resistant organisms, yadda yadda. So you make do with some Tylenol®, cough syrup, and resign yourself to a few lousy days of suffering.

Five days into your illness, you’ve not shown up for work, you’re having trouble breathing, and you’re getting delirious. An emergency trip to the hospital follows, where a bronchoscopy is performed (an imaging scope threaded down your airway) and organisms recovered for diagnosis. You’re put on a ventilator through a tube in your throat to support your breathing and treated with intravenous antibiotics. Delayed treatment permits infection to escape into the fluid around your lungs, creating an “empyema,” an extension of the infection that requires insertion of a tube into your chest through an incision to drain the infection. You require feeding through a tube in your nose, since the ventilator prevents you from eating through your mouth. After 10 days, several healing incisions, and a hospital bill totaling $75,000, you’re discharged only to be face eights weeks of rehabilitation because of the extreme toll your illness extracted. Your doctor also advises you that, given the damage incurred to your lungs and airways, you will be prone to more lung infections in the future, and similar situations could recur whenever a cold or virus comes long.

A disease treatable by taking a two week, $20 course of oral antibiotics at home has been converted into a lengthy hospital stay that generated extravagant professional fees, testing, and costly supportive care. You’ve lost several weeks of income. You’re weak and demoralized, frightened that the next flu or virus could mean another trip to the hospital.

Such a scenario would be unimaginable with a common infection like pneumonia, or it would be grounds for filing a malpractice lawsuit. But, as horrific as it sounds in another sphere of healthcare, it is, in effect, analogous to how heart disease is managed in current medical practice.

First, you’re permitted to develop the condition. It may require years of ignoring the telltale signs, it may require your unwitting participation in unhealthy lifestyle choices. Palliative treatments that slow, but don't stop, the progression of disease are prescribed like cholesterol drugs. The process then eventuates in some catastrophe like heart attack or similar unstable heart situation, at which point you no longer have a choice but to submit to major heart procedures. That’s when you receive your heart catheterization, coronary stents, bypass, defibrillators, etc. and you're proudly declared a "success" of medical technology.

Of course, none of these procedural treatments cures the disease, no more than a Band Aid® heals the gash in your leg. The conditions that were present that created your heart disease continue, allowing a progressive disease to worsen. At some point, you will need to return to the hospital for yet more procedures when trouble recurs, which it inevitably does.

A coronary bypass operation costs, on average $85, 653 (AHA 2008 Update; based on 2004 data). That doesn't include the $25,433 cost for the heart catheterization performed by a cardiologist to provide the surgical roadmap of your coronary arteries. If there are any complications of your procedure, then your hospital bill may total a substantially higher figure.

$85, 653 is just the upfront financial pay-off. Over the long run, your life is actually worth far more to the cardiovascular healthcare system because no heart procedure yields a permanent fix. In fact, repeated reliance on the system is the rule.

In fact, over 90% of people who enter the American cardiovascular healthcare system do so through a revolving door of multiple procedures over several years. It is truly a rare person, for instance, who undergoes a coronary bypass operation, never to be seen again the wards of the hospital because he remains healthy and free of catastrophe. A much more familiar scenario is the man or woman who undergoes two or three heart catheterizations, receives 3,4, or 6 stents, followed a few years later by a heart bypass, pacemaker, defibrillator, as well as the tests performed for catastrophe management, such as nuclear stress test, echocardiogram, laboratory blood analysis, and consultation with several specialists. Re-do bypass surgeries--a 2nd, 3rd, or 4th bypass--now comprise 25% of all bypass procedures.

The total revenue opportunity is many-fold higher than the initial 80-some thousand dollars, but instead totals hundreds of thousands of dollars per person.

What motivation can there possibly be to 1) identify coronary disease early, when in its asymptomatic stage, then 2) identify its causes, then 3) correct the causes, and finally 4) shut off the disease? You and I can accomplish this with a few hundred dollars of cost, perhaps a few thousand over many years (to cover costs of fish oil, vitamin D, niacin, and whatever else it takes to stop the expression of the disease). Nobody therefore profits substantially from your prevention effort--except you.

Then what if nobody told you that heart disease could be managed this way? That's what I mean by "disease engineering."

Dr. Steven Gundry on The Livin' La Vida Low-Carb Show

20. October 2008 William Davis (4)

I stumbled on a great interview with cardiothoracic surgeon, Dr. Steven Gundry, on Jimmy Moore's Livin' La Vida Low-Carb Show. (Or, cut and paste: http://www.thelivinlowcarbshow.com/dr-steven-gundry-part-1-episode-179/)

Dr. Gundry has some fun ways of looking at eating and health. I found his comments on the activation of genes (discussed at a very light, non-scientific level) useful. He argues that when humans consume sugar-containing foods, the signal received by the body is that winter is approaching and it's time to build up fat stores in anticipation of the food shortages of cold weather. He finds parallels for this phenomenon in other species. Of course, for humans, winter (in the form of extended calorie deprivation) never comes. In fact, you might argue that, given our excessive reliance on grains, corn, and sugars, that we are, in effect, always in anticipation of a winter that never comes.

I've not read Dr. Gundry's books, but I found this light interview a lot of fun.

Does fish oil ADD to statin therapy?

18. October 2008 William Davis (9)

Yet another patient came to my office today saying, "My primary doctor said that I should stop taking fish oil. He say's that I don't need it because I take Crestor."

The woman was in tears, confused and frightened over a potential disagreement between her doctors.

Is this true? If someone takes a statin drug, like Crestor, Lipitor, Zocor (simvastatin), pravachol, or lovastatin, they don't need to take anything else because the statin drug is so powerful that it eliminates risk?

No. Not even close to the truth.

First of all, let's accept that virtually the entire body of statin drug literature--hundreds of studies, billions of dollars spent--was paid for by the drug industry. It's no news that studies paid for by the sponsor are likely to favor the sponsor. Imagine Ford sponsored a study of Ford vs. GM cars vs. Toyota, paying $10 million to fund the effort. Guess who is likely to come out on top? "Studies show that Ford makes the best car in America." (Sorry, I don't mean to pick specifically on Ford. It's just a widely-recognized brand.)

So that means that the statin literature likely overestimates the benefit of statin drugs. Even so, it's clear from the hundreds of studies performed that the best we can hope for by taking statin drugs is a reduction of heart attack and death from heart attack of 30-35%--best case. That doesn't sound like elimination of risk to me.

What are the incremental benefits of adding omega-3 fatty acids from fish oil added to statins? The best data originate with the JELIS Trial (Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis), in which 19,000 Japanese participants (who already have a high omega-3 intake from diet, usually ranging from 1800-3000 mg per day) experienced a 19% reduction (relative reduction) in cardiovascular events.

GISSI Prevenzione demonstrated a 28% reduction in heart attack, 45% reduction in death from heart attack with fish oil.

Omega-3 fatty acids from fish oil also:

--Reduce triglycerides dramatically
--Accelerate after-eating clearance of digestive by-products, i.e., they correct post-prandial abnormalities
--Modify the character (fragmentation potential, structural strength) of plaque
--Raise HDL modestly

If you buy your fish oil from Sam's Club, Costco, or other discounter, a healthy dose of fish oil might cost you $3 per month. Compare that to the $120 per month average cost of a statin agent. Why is there even a discussion over this?

Sadly, the doctor on Main Street, U.S.A, is the unwitting puppet of the pharmaceutical industry. The pretty drug company representative with nice legs and a cute smile promises lunch, dinner and . . who knows what else? Wink. The fifty-something, hairline-receding doctor can't resist. "Of course I'll prescribe your drug!"

Don't kid yourself: The drug industry knows precisely how to manipulate the behaviors of the deliverers of their products.

So, do statin drugs make omega-3 fatty acids from fish oil irrelevant? Absolutely not.

It's all about trying to inch closer and closer--not to reduction--but to elimination of risk for heart disease.

HDL: “H” is for “happy”

16. October 2008 William Davis (10)

What role do emotions play in HDL cholesterol?

I’ve often observed a peculiar phenomenon: People who come to the office or hospital in the midst of a difficult emotional situation-e.g., stress at home, financial struggles, hospitalization (usually an unhappy occasion)- can show dramatic drops in HDL cholesterol. Not uncommonly, HDL drops 20 or more mg/dl.

Take Agnes’s case. Agnes had to go to the hospital for an elective procedure, one she’d been dreading for months. Previously, Agnes had been proud of the fact that she’d incrased HDL from 42 mg/dl range all the way up to 71 mg/dl. She accomplished this dramatic increase by eliminating wheat and cornstarch from her diet (which helped her lose 24 lbs), taking vitamin D and omega-3 fatty acids from fish oil, exercise, 2 oz of dark chocolate per day, and a glass of red wine with dinner.

Although I wouldn’t have bothered checking a cholesterol panel for such a procedure, the hospital had a checklist that included a cholesterol panel regardless of necessity. (Such checklists are common in hospitals, meant to ensure that certain basic issues are not overlooked.)

Agnes’ HDL: 29 mg/dl-a 42 mg drop.

Agnes will recover and her HDL will rebound, but the same effect can occur with other stressful situations, such as death in the family, financial worries, marital stress, etc., as well as physical illness.

Interestingly, the opposite may also hold true: Low HDL may increase risk for depression and stress. A study from Finland of 124 depressed persons, for instance, showed a 240% increased likelihood of depression in those with lower HDL cholesterols.

In other words, there seems to be a curious interdependence between HDL and emotions.

Why? Does it represent the indirect effect of adrenaline, cortisol, or other “stress hormones”? Do factors that relate to low HDL, such as unhealthy diet full of carbohydrates and physical inactivity, also tend to cultivate depression?

It certainly seems to be a chicken-egg situation, with one often leading to the other.

Moral of the story: Maintaining a sense of optimism and engaging in activities that bring you satisfaction and enjoyment can help raise HDL, as can strategies such as those followed by Agnes. Avoiding unnecessarily stressful situations can help. HDL is important, since higher levels are associated with much reduced risk for heart disease . . . and perhaps depression.

Plaquology

13. October 2008 William Davis (3)

Plaquology: A new term.

Plaquology: def: (plaque-: atherosclerotic plaque; -ology: study of.) The study of atherosclerotic plaque, originating in the early 21st century during the time period when the material underlying atherosclerosis gained recognition as a measure superior to "risk factors" for cardiovascular disease. Previous to the plaque concept, blood measures of cholesterol and adverse lifestyle habits, such as smoking and sedentary lifestyle, alone had been used to predict potential for cardiovascular events. With acceptance of the concept of plaque measurement, the concept of risk factors was abandoned.

Look it up in the current Oxford Dictionary of the English Language, or Webster's Dictionary, and I'm afraid that you still won't find plaquology . . . but you should.

I'm currently rewriting many parts of the Track Your Plaque book. The rewriting process has caused me to review just how much we've learned these past few years. One of the phenomena that fascinates me is that we now have non-medical people--teachers, software people, engineers, bankers, bed and breakfast owners, retired businesspeople, etc.--all discussing the finer points of coronary atherosclerotic plaque--plaquology--what constitutes plaque, what triggers plaque inflammation, how to quantify potential for plaque rupture or plaque quiescence, what effect various treatments have on plaque composition and behavior, etc.

We now have a legion of Plaquologists!

I'm very proud of our Plaquologists. Having devoted themselves to the study of plaque, their level of knowledge now exceeds that of 99% of practicing physicians, including my colleagues, the cardiologists. While cardiologists spend their day squashing/cutting/vaporizing plaque, they are no more experts in plaquology than a carpenter is an expert in trees. More often than not, cardiologists view plaque as just something that gets in their way, rather than the quantifiable, modifiable, reversible material that we can exert control over.

One of the software tools currently in the works for the Track Your Plaque website is a certification process. Members will be able to gain a "certification" in various topics relevant to plaquology, such as plaque quantification, lipoprotein testing, and nutritional supplements.

How about a Doctor of Plaquology?

Thyroid perspective update

10. October 2008 William Davis (18)

Since the publication of the extraordinary HUNT Study relating the entire spectrum of thyroid function and heart issues, I have been vigorously and systematically examining thyroid function in numerous patients.

While there's no news in relating flagrant low thyroid function with triggering heart disease in several forms, the cut-off between low thyroid and normal thyroid has been a matter of dispute for decades.

In the early 20th century, low thyroid function wasn't diagnosed until someone gained 40 lbs, displayed extravagant amounts of edema (water retention) in the legs and huge bags under the eyes, hair fell out in clumps, and often eventually proved fatal. At autopsy, these unfortunates also showed advanced and extensive quantities of coronary atherosclerotic plaque.

Low thyroid is usually diagnosed on the basis of the blood test, thyroid stimulating hormone, or TSH. TSH is a pituitary gland hormone responsible for stimulation of thyroid function. When thyroid function flags, the pituitary increases TSH release. Thus, a high TSH signals lower thyroid hormone levels.

The difficulty is in distinguishing normal thyroid function from low thyroid function judged by TSH levels. As the years have passed, in fact, the cut-off for "normal" TSH has drifted lower and lower.

The HUNT Study, I believe, clinches the argument: A TSH of 1.5 or lower, perhaps even 1.0 or lower, is desirable to eliminate the excess cardiovascular risk provided by an underactive thyroid, not to mention feel better: more energetic, clearer thinking, greater well-being.

Having now applied this renewed appreciation for thyroid, I have come to believe that:

--Low thyroid function, even subtle levels, are rampant and far more common than ever previously thought. In my office practice, the case could be made that several people per day are marginally or mildly hypothyroid (low in thyroid).
--Restoration of optimal thyroid levels facilitates correction of lipid measures, especially LDL cholesterol and, to a lesser degree, lipoprotein patterns dependent on the insulin axis such as triglycerides and small LDL. It's a lot happier way to correct lipids than statins.

I don't discount the value of feeling better. People who feel better--more energetic, more upbeat, clearer thinking--tend to do better in health overall. If thyroid restoration is a part of that equation, then greater attention should be paid to this facet of health on our way to optimal heart health.

Though I sometimes feel like an endocrinologist dispensing desiccated thyroid (rarely the synthetic T4), I believe that this has been a previously neglected and important part of our effort to achieve coronary plaque stabilization and reversal.

Accidental Health

9. October 2008 William Davis (2)

"I shall never have smallpox for I have had cowpox; I shall never
have an ugly pockmarked face."

Such was the idle comment made by a milkmaid to Edward Jenner in 1768 when Jenner was 19, a remark that later prompted his investigations into using isolates of cowpox injected into humans as the first vaccination against the devastations of the European epidemic of smallpox.

(A caricature of Jenner administering cowpox vaccine to people, causing them to sprout bovine appendages. Image courtesy Wikipedia and the Library of Congress.)

When I look back, something similar has happened here.

Although the Track Your Plaque program is intended to stop and reverse coronary plaque using the only available means of tracking coronary plaque, i.e., heart scans, an unintended panel of benefits follow:

--People lose weight, often dramatically
--People gain greater energy
--Thinking is clearer, emotions more stable
--Sleep is deeper
--Bone density increases
--Physical strength and coordination improve
--Winter blues dissipate
--Blood sugar drops dramatically
--Blood pressure drops

Cholesterol (lipid) panels also settle to values that most physicians deem impossible or impractical, given our target of 60:60:60, i.e., LDL 60 mg/dl or less, HDL 60 mg/dl or higher, triglycerides 60 mg/dl or less. And medications are not always necessary to achieve these values. (When I show these values to my colleagues, they declare them flukes, unobtainable only in select people with high doses of medications.)

I didn’t set out to find the next weight loss solution, nor the key to boundless energy. My goal was "simpler": create a program of heart health. I am, after all, a cardiologist.

I was so intently focused on achieving incremental improvements over the steps leading to heart disease prevention that I failed to recognize the profound phenomena that accompanied it: people were quicker, smarter, thinner, and healthier.

In other words, I believe that we have inadvertently created a program of super health and performance.

Ironically, most people don't want to talk about heart disease, let alone reversal of heart disease. They do want to talk about getting thinner, feeling more energetic, living longer, better cholesterol values, etc.

Perhaps there's a lesson in this.

Livin' La Vida Low Carb interview

7. October 2008 William Davis (5)

I recently provided an interview for Livin' La Vida Low Carb's irrepressible Jimmy Moore.

Jimmy runs a fun set of blogs, webcasts, and the like to broadcast this message of reducing carbohydrates in the diet. He credits his 210 lb weight loss to a strict low-carbohydrate and exercise program.

For the interview, just go to The Livin' the Vida Low Carb Show, Episode 185, or click here.

And click here for Part 2

For more of Jimmy Moore's spin on the entire low-carbohydrate diet experience, he maintains several popular blogs, including Carb Wire and The Livin' La Vida Low-Carb Blog.

Wheat withdrawal: How common?

5. October 2008 William Davis (11)

In response to the recent Heart Scan Blog poll,

Have you experienced fatigue and mental fogginess with stopping wheat, i.e., "wheat withdrawal"?

the 104 respondents said:

Yes, I have experienced it: 26 (25%)

No, I stopped wheat and did not experience it: 65 (62%)

I'm not sure: 3 (2%)

I haven't tried it but plan to: 7 (6%)

I haven't tried it and don't plan to: 3 (2%)

So 25% of respondents reported experiencing the fatigue and mental fogginess of wheat withdrawal. This is similar to what I observe in my practice.

I counsel many patients to consider the elimination of wheat, as well as cornstarch products, in an effort to regain control over:

--Weight
--Appetite
--Low HDL
--High triglycerides
--Small LDL
--High blood sugar
--High blood pressure

All of these issues respond--often dramatically--to elimination of wheat and cornstarch.

Why would there be undesirable effects of eliminating wheat?

One clear issue is that elimination of wheat and other sugar-equivalents deprives your body of glucose. Your body then needs to resort to fatty acid metabolism to generate energy. Apparently, some people are inefficient at this conversion, having subsisted on carbohydrates for the last few decades of their lives. However, as fatty acid metabolism kicks in, energy generation improves. That is my (over-)simplified way of reasoning it through.

However, are there other explanations behind the mental fogginess, drop in energy, and overwhelming sleepiness? Some readers of this blog have suggested that, since opioid-like sequences (i.e., amino acide sequences that activate opiate receptors) are present in wheat, perhaps withdrawal from wheat represents a lesser form of opiate withdrawal. I find this a fascinating possibility, though I know of no literature devoted to establishing a cause-effect relationship.

Whatever the mechanism, I find it very peculiar that this food widely touted by the USDA, American Heart Association, and other agencies actually triggers a withdrawal syndrome in approximately 25% of people. Spinach does not trigger withdrawal. Nor does flaxseed, olive oil, almonds, and countless other healthy foods.

Then why would whole wheat grains be lumped with other healthy foods?

Treat the patient, not the test

5. October 2008 William Davis (0)

"Treat the patient, not the test."

That is a common "pearl" of medical wisdom often passed on during medical training.

It refers to the fact that we should always view any laboratory or imaging test in the context of the live, human patient and not just treat any unexpected value that doesn't seem to make sense.

I raise this issue because it recently came up on a discussion on the Track Your Plaque Forum. A Member with a high heart scan score of around 1100 was advised by his doctor that it should be ignored, because he'd prefer to treat the patient, not the test. The patient is apparently slender, physically active, and entirely without symptoms, with favorable cholesterol values as well. The high heart scan score didn't seem to jive with the appearance of the patient, as viewed by this doctor.

This common phrase is meant to impart wisdom. It is a reminder that we treat real people, not just a jumble of laboratory values.

But the unspoken part of the equation is that judgment needs to be applied. A well looking person who shows an unexpected rise in white blood cell count could just have a screwy result, or could have leukemia. Liver tests (AST, ALT) that top 400 could represent a fluke, or dehydration incurred during a long workout, or hepatitis from a long ago blood transfusion.

Yes, treat the patient. But don't be an idiot and entirely dismiss the signficance of an unexpected laboratory or imaging test. A heart scan score of 1100 should be as readily dismissed as discovering a white blood cell count of 90,000 (normal is less than 12,000), or a 5 cm mass in the lung. The absence of symptoms or the failure of conventional risk factors to suggest causation is insufficient reason to dismiss the concrete findings of a test.

In this particular person, dismissing the significance of the heart scan finding by suggesting that the doctor should treat the patient, not the test, is tantamount to:

--Colossal ignorance
--Malpractice
--A certain sentencing of the hapless patient to future major heart procedures, heart attack or death (20-25% likelihood every year, or a virtual certainty over the next 5 years).

There is an ounce of wisdom in this old medical pearl. But there's also plenty of room for a knuckleheaded doctor to misconstrue and abuse its meaning for the sake of covering up his/her ignorance, laziness, or lack of caring.

The Big Squeeze

20. June 2008 William Davis (5)

Some colleagues of mine brought this scary phenomenon to my attention last evening.

As insurance and Medicare reimbursement to doctors and hospitals fall (Medicare is enacting a series of substantial cuts, which will be followed by the private health insurers), you would expect the use of hospital procedures to drop. Makes sense, right? Less money paid per procedure, less incentive to do them.

Unfortunately, that's not how it's playing out in the real world. Your neighborhood interventional cardiologist or cardiothoracic surgeon is accustomed to a level of income and lifestyle. That lifestyle is now threatened by shrinking reimbursement. True to the Law of Unintended Consequences, rather than reducing use of procedures, diminishing procedural fees are prompting a good number of practitioners to do more.

In other words, if each heart catheterization pays less, why not do more of them, along with more stents, pacemakers, defibrillators, and the like? If four heart catheterizations per day pays less, why not do five to make up the difference?

Voila! Income protected. Of course, it comes at the cost of more work. But I will give one thing to my colleageus: They are a generally hard-working bunch who rarely balk at 12-16 hours days in the hospital.

How do you do more procedures? Easy. Just lower the bar on who to do a procedure on. Use more aggressive criteria for pacemaker implantation. Interpret the always-fuzzy nuclear stress tests weighed more towards abnormal. Use scare tactics: "You never know--that chest pain could be the last warning you're going to have!" Because the criteria for performing procedures is "soft" in the real world, it is easy to bend the criteria any way you want.

It's too early to measure the full impact of this unintended consequence of reduced reimbursement. But don't allow yourself to become a casualty in the reimbursement war. Remain vigilant. Recognize that, despite the fuzziness at the edges, there are still rational reasons for performing heart procedures. Always be armed with information and the right questions. Never submit unquestioningly or without satisfactory answers to your questions.

Tim Russert's heart scan score 210. . .in 1998

18. June 2008 William Davis (10)

Despite the media blathering over how Mr. Russert's tragic death from heart attack could not have been predicted, it turns out that he had undergone a heart scan several years ago.

A New York Times article, A Search for Answers in Russert’s Death, reported:

Given the great strides that have been made in preventing and treating heart disease, what explains Tim Russert’s sudden death last week at 58 from a heart attack?

The answer, at least in part, is that although doctors knew that Mr. Russert, the longtime moderator of “Meet the Press” on NBC, had coronary artery disease and were treating him for it, they did not realize how severe the disease was because he did not have chest pain or other telltale symptoms that would have justified the kind of invasive tests needed to make a definitive diagnosis. In that sense, his case was sadly typical: more than 50 percent of all men who die of coronary heart disease have no previous symptoms, the American Heart Association says.

It is not clear whether Mr. Russert’s death could have been prevented. He was doing nearly all he could to lower his risk. He took blood pressure pills and a statin drug to control his cholesterol, he worked out every day on an exercise bike, and he was trying to lose weight, his doctors said on Monday. And still it was not enough.

“What is surprising,” Dr. Newman said, “is that the severity of the anatomical findings would not be predicted from his clinical situation, the absence of symptoms and his performing at a very high level of exercise.”

Buried deeper in this article, the fact that Mr. Russert had a heart scan score of 210 in 1998 is revealed.

That bit of information is damning. Readers of The Heart Scan Blog know that heart scan scores are expected to grow at a rate of 30% per year. This would put Mr. Russert's heart scan score at 2895 in 2008. But the two doctors providing care for Mr. Russert were advising the conventional treatments: prescribing cholesterol drugs, blood pressure medication, managing blood sugar, and doing periodic stress tests.

Conventional efforts usually slow the progression of heart scan scores to 14-24% per year. Let's assume the rate of increase was only 14% per year. That would put Mr. Russert's 2008 score at 779.

A simple calculation from known information in 1998 clearly, obviously, and inarguably predicted his death. Recall that heart scan scores of 1000 or greater are associated with annual--ANNUAL--risk for heart attack and death of 20-25% if no preventive action is taken. The meager prevention efforts taken by Mr. Russert's doctors did indeed reduce risk modestly, but it did not eliminate risk.

We know that growing plaque is active plaque. Active plaque means rupture-prone plaque. Rupture prone plaque means continuing risk for heart attack and death. Heart attack and death means the approach used in Mr. Russert was a miserable failure.

While the press blathers on about how heart disease is a tragedy, as Mr. Russert's doctors squirm under the fear of criticism, the answers have been right here all alone. It sometimes takes a reminder like Mr. Russert's tragic passing to remind us that tracking plaque is a enormously useful, potentially lifesaving approach to coronary heart disease.

Who needs to go next? Matt Lauer, Oprah, Jay Leno, some other media personality? Someone close to you? Can this all happen right beneath the nose of your doctor, even your cardiologist?

I don't need to remind readers of The Heart Scan Blog that heart disease is 1) measurable, 2) trackable, 3) predictable. Mr. Russert's future was clear as long ago as 1998. Every year that passed, his future became clearer and clearer, yet his doctors fumbled miserably.

Copyright 2008 William Davis, MD

Another failure of conventional cardiac care

15. June 2008 William Davis (5)

Though Tim Russert was widely known and respected for his political commentary, he will likely be better remembered as an example of the gross shortcomings of the conventional approach to heart disease.

Let's face it:

Standard heart disease prevention efforts are a miserable failure.

A Track Your Plaque member brought this interview of Mr. Russert's doctor to my attention.

It appears that his doctor did all the correct conventional things. You know what became of it. In the eyes of the public and of any attorney, or even of my colleagues, no wrong was committed. The blame does not lie with Mr. Russert's hapless doctor. The blame lies on the system that endorses procedures, prescription medications, the blind adherence to dogma dictated by the pharmaceutical industry and FDA, along with a prevailing philosophy of preferring the management of catastrophes to preventing them. Dr. Newman's idea of a solution: Making an automatic defibrillator (AED) more widely available (!!!).

How long does this sort of idiocy have to go on? How many people have to die before the system uses the tools that are already available, tools that could have prevented this tragedy and many more like it?

If you and your doctor subscribe to the program that the unfortunate Mr. Russert was prescribed and the brainwashing, unthinking nonsense that his doctor follows, you are a fool. Shame on you. You therefore likely subscribe to the same variety of marketing BS that issues from food manufacturers about Cheerios, whole grains, and low-fat diets.

Get with the program. Sadly, Mr. Russert is not the first, he's not the last. The tragedies of conventional advice that line the pockets of drug and food manufacturers number in the millions. We're not talking about some obscure, rare disease. We're talking about the number one cause of death in both males and females nationwide.

I deeply wish this message could have reached Mr. Russert before his untimely death. We could all look forward to another Sunday morning with his usual incisive, unforgiving probing of the day's political figures.

Tribute to Tim Russert

14. June 2008 William Davis (11)

The sudden passing of news giant, Tim Russert, yesterday of sudden cardiac death struck a blow to American consciousness.

Perhaps his hard-hitting interviewing style, while making guests squirm, made him seem invincible. But, of course, none of us is invincible. We are all vulnerable to this disease.

We should not allow Mr. Russert's tragic death to occur without taking some lessons. The media have already resorted to interviewing prominent doctors for their opinion.

Douglas Zipes, M.D., former President of the American College of Cardiology,was quoted in the media:

"An automated external defibrillator (AED) could have been a life-saver. AEDs should be as common as fire extinguishers."

This is typical sleight-of-hand, medicine-is-too-complex-for-the-public-to-understand sort of rhetoric that is surely to issue from the conventionally-thinking medical people and the press. Instead, let's cut the BS and learn the real lessons from Mr. Russert's needless death.

It is virtually certain that:

--Mr. Russert ruptured an existing coronary atherosclerotic plaque, prompting rhythm instability, or ventricular fibrillation.

--Making automatic external defibrillators (AED) available might have Band-Aided the ventricular fibrillation, but it would not have stopped the heart attack that triggered it.

--Though full details of Mr. Russert's health program have not been made available, it is quite likely that he was prescribed the usual half-witted and barely effective panoply of "prevention": aspirin, statin drug, anti-hypertensive medication. Readers of The Heart Scan Blog and members of Track Your Plaque know that this conventional approach is as effective as aspirin for a fractured hip.

--It is highly unlikely that all causes of Mr. Russert's heart disease had been identified--did he have small LDL (it's certain he did, given his body habitus of generous tummy), Lp(a), low HDL, pre-diabetic patterns, inflammatory abnormalities, vitamin D deficiency, etc.? You can be sure little or none of this had been addressed. Was he even taking simple fish oil that reduces the likelihood of sudden cardiac death by 45%?

--Far more could have been done to have prevented Mr. Russert's needless death. And I don't mean the idiocy of making AED's available in office buildings. I'm talking about preventing the rupture of atherosclerotic plaque in the first place.

Far more can be done to prevent future similar deaths among all of us.

Our jobs are to use the tragic death of Mr. Russert to help those around us learn that heart disease is identifiable and preventable. Though Mr. Russert did not stand for BS in his political commentary, he sadly probably received it in his health advice. Don't let this happen to you or those around you.

Why do skinny people get heart disease?

13. June 2008 William Davis (9)

There's no doubt about it: The majority of people with heart disease are overweight. They may not be grotesquely overweight, just a few pounds over. But weight plays a crucial role in activating numerous factors that heighten risk for heart disease.

Excess weight reduces HDL cholesterol, raises triglycerides, increases small LDL (enormously), fans the fires of inflammatory responses (CRP, IL-6, TNF-alpha, etc.) raises blood pressure, increases resistance to insulin and raises blood sugar. Overweight people tend to be less physically active, may develop diseases of obesity like sleep apnea, and on and on. You've heard this all before.

But why do slender people develop heart disease? If we can't blame weight, what is to blame? By slender, I mean body mass index (BMI) of <25. (Yes, I know there are other ways, better ways, to gauge healthy weight. But, for simplicity, I'll use BMI.) Let's put aside the two obvious causes of heart disease, cigarette smoking and Type I diabetes. (I'd be shocked if any cigarette smokers read this blog.)

Slender people develop heart disease because:

1) They have lipoprotein(a)--The big, big neglected risk factor. In fact, the Lp(a) genotype is, in my casual observation, associated with a slender phenotype (genotypic expression). The prototypical example that makes headlines is the marathon runner--slender and superbly fit, but develops heart disease anyway. People wax on about the uncertainties of exercise and fitness when they hear about Jim Fixx and Alberto Salazar. But one factor would explain it all: Lp(a).

2) The murky category of the normal weight obesity. These people are generally recognizable by their flaccid tummies despite falling into a favorable BMI <25. Small LDL is the standout red flag in these people.

3) They were previously overweight but lost it.

4) They were former smokers.

5) Vitamin D deficiency--Deficiency of vitamin D is important for everyone's health. But there appears to be some people for whom it is the dominant risk. I believe that one of our great Track Your Plaque success stories, Neal, falls into this group. Some people who are vitamin D deficient develop colon cancer, others develop diabetes, others develop osteoporosis or multiple sclerosis, while others develop coronary heart disease and plaque. The likely reason for the varied expression is variation in vitamin D receptor genotypes (VDR genotypes).

6) The murkiest of all: Hypertension genotypic variants. This is a poorly sorted-out category, and one principally based on my observations along with scattered observations in such things as variations in the angiotensin converting enzyme genotypes. But I am convinced that there is a small percentage of slender people who show variation in some genetic type that predisposes to hypertension and heart disease. They also show a propensity towards enlargement of the thoracic aorta. This group is also among the most difficult to control in the Track Your Plaque approach, i.e., they have difficulty slowing or stopping the growth of heart scan scores. While blood pressure control in this group is important, it does not seem to remove the excess source of risk.

So, yes, being slender does put you into a lower risk for heart disease category. But it does not mean you are immune.

You can also be an overweight person who still harbors some of the features of the slender--you're an overweight slender person. The above list can still therefore apply.

Cardiology Confidential

11. June 2008 William Davis (9)

Okay, so it's a shameless knockoff of chef Anthony Bourdain's titillating Kitchen Confidential.

But the confidences that I've heard whispered in the corridors of health involve something more provocative than how your food was prepared. Any service for humans performed by other humans is subject to the idiosyncrasies and weaknesses of human behavior. That's just life.

In healthcare for your heart, the consequences can be more profound than eating three day old fish on Monday's dinner menu.

Over my 15 years practicing cardiology in a variety of settings in three different cities, I've witnessed just about everything from shocking to sublime. Some of it speaks to the extraordinary commitment of people in healthcare, the unexpected courage people show in the midst of illness, the devotion of family in difficult times. It can also speak of mewling, sobbing carryings-on over the most minor conditions, the meanness that emerges when people are frightened, the vultures circling just waiting for Grandpa to kick the bucket and leave his will declaring the spoils.

For the most part, my cardiology colleagues are a hard-working bunch committed to . . . Uh oh. I was going to say "Saving lives, preserving health." But that's not true. Once upon a time, it was true for many of my colleagues, often revealed over $2-a-pitcher beer-softened, "we're going to save people" conversations in medical school. Ahhh, medical school. I remember walking along the street alongside my medical school in St. Louis, bursting with pride and a sense of purpose.

But, for many of us, something sours our purpose through the years. Maybe it's the smell of money, maybe it's the series of distasteful experiences that show that healthcare providers are, in the midst of health crises, the innocent recipients of anger, frustration, disappointment.

Whatever the genesis, the stage is set for an imperfect scenario that pits healthcare provider against patient in a less-than-perfect system.

This would read as a mindless rant if it wasn't based on such pervasive and pravalent truths, tales of the flawed deliverers of healthcare driven by motives less lofty than "saving people."

Take Dr. S, a doctor who performs a large number of procedures on patients. I'm told he is very capable. He manages an extraordinary amount of heart work--in between jail time for wife beating and Medicare fraud.

Or Dr. C, well-known in the region for his procedural talents, also. Usually acerbic and freely-swearing, he opens up engagingly when drinking--which is most of the time. Paradoxically, as is true for some serious drinkers, he works more effectively while intoxicated.

Or Dr. ST, who proudly admitted to me one evening over dinner that he has accepted 6-figure payments from medical device companies on a number of occasions to use their products.

Or the manic ups and downs of Dr. J, who refers just about every patient he sees for emergency bypass surgery when in his down phase, mangles coronary arteries in daring angioplasties during his up phase.

How about 310-lb Dr. P, who hounds her patients about indulgent lifestyles? That would be excusable as innocent lack of self-insight if it weren't for her propensity to use heart procedures on patients as punishment. "I have no choice but to take you to the hospital."

Dr. M. manages to maintain the appearance of straight-and-narrow during the day, all the way to attending church twice a week with his children. His daytime persona effectively covers up his frequent visits to prostitutes.

We are ALL flawed. My colleagues are no different. But some circumstances cultivate the flaws, fertilize corruptibility, reward it. Such has become the state of affairs in healthcare for heart disease. Why? Is it the excessive potential for money-making that existed until recently? Is there something about the save-the-day mentality of heart disease that attracts imperfect personalities looking for the adrenaline-charged thrill but morphs over time into near-psychopathic lives?

It's not the end of the world. The fact that my colleagues' behavior has reached such extravagant lows signals a bottom: things are about to change.

In the meantime, let me tell you a few more secrets . . .

Copyright 2008 William Davis, MD

Fanatic Cook on the American Heart Association

8. June 2008 William Davis (7)

The Fanatic Cook has posted a stinging criticism of the American Heart Association (AHA):

American Heart Association My Fat Translator

Beyond the nonsensical nutritional recommendations (e.g., substitute small French fries for large French fries), she lists the major financial contributors to the AHA, a Who's Who in the pharmaceutical and processed food industry.

"For an organization that brought in close to a billion dollars last year, you'd think they could come up with something a little more pronounced. If I was more cynical I'd say the AHA had an interest in keeping Americans fat . . . or at least dependent on a highly-processed, fast food diet, requiring drugs to tweak lab values."

To be sure, the AHA does a great deal of good in funding research and educating the public about the prevalence of heart and vascular disease. But their fund raising interests have clearly subverted the honesty of their nutritional advice. Sadly, it is the AHA dietary advice that hospital dietitians use in counseling people with heart disease after their heart attack, stent, or bypass surgery. After my patients are discharged from the hospital for any reason, I tell them to please forget everything the nice hospital dietitian told them. It is not okay to eat the factory farm-raised hamburger on the sugar-equivalent enriched flour bun. Low-fat ice cream is not a healthy substitute for full-fat ice cream.

The AHA is no different than the USDA and the American Diabetes Association, "official" organizations that have, in effect, sold out to industry.

Sleep for heart health

8. June 2008 William Davis (4)

Sleep is a fascinating phenomenon.

Virtually all animals, certainly all mammals, sleep. While the form and shape of sleep can vary, sleeping is a universal phenomenon. Even fish sleep, though their eyes remain open.

Sleep disorders like sleep apnea ("apnea" = without breathing) are growing in prevalence nationwide as the country gets fatter and fatter. Our throats assume a smaller diameter, even our tongues get obese. This results in intermittent obstruction to the airway during sleep, causing snoring. It also results in sleep interruption, particularly during attempts to "descend" down to the deepest phases of sleep. Dire health and cardiac consequences can sometimes emerge, such as high blood pressure, higher blood sugar, abnormal heart rhythms, impaired heart muscle function, even sudden death.

We are all familiar with the perceptible effects of sleep deprivation: edginess, crabbiness, diminished attention span, slowed reaction time. I'm not talking about sleep apnea or sleep disorders, but just simple duration of sleep. Data are emerging that both sleep deprivation and sleep excess may trigger undesirable changes in lipids (cholesterol values):

Associations of usual sleep duration with serum lipid and lipoprotein levels.

Kaneita Y, Uchiyama M et al.

STUDY OBJECTIVES: We examined the individual association between sleep duration and a high serum triglyceride, low HDL cholesterol, or high LDL cholesterol level. DESIGN AND SETTING: The present study analyzed data from the National Health and Nutrition Survey that was conducted in November 2003 by the Japanese Ministry of Health, Labour and Welfare. This survey was conducted on residents in the districts selected randomly from all over Japan. PARTICIPANTS: The subjects included in the statistical analysis were 1,666 men and 2,329 women aged 20 years or older. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Among women, both short and long sleep durations are associated with a high serum triglyceride level or a low HDL cholesterol level. Compared with women sleeping 6 to 7 h, the relative risk of a high triglyceride level among women sleeping <5 h was 1.51 (95% CI, 0.96-2.35), and among women sleeping > or =8 h was 1.45 (95% CI, 1.00-2.11); the relative risk of a low HDL cholesterol level among women sleeping <5 h was 5.85 (95% CI, 2.29-14.94), and among women sleeping > or =8 h was 4.27 (95% CI, 1.88-9.72). On the other hand, it was observed that the risk of a high LDL cholesterol level was lower among men sleeping > or =8 h. These analyses were adjusted for the following items: age, blood pressure, body mass index, plasma glucose level, smoking habit, alcohol consumption, dietary habits, psychological stress, and taking cholesterol-lowering medications. CONCLUSIONS: Usual sleep duration is closely associated with serum lipid and lipoprotein levels.

Triglycerides go up with too little or too much sleep. Note especially the extraordinary association of low HDL cholesterol with sleeping <5 hours (nearly 6-fold increased risk) or sleeping >8 hours (more than 4-fold increased risk).

Why do these effects develop? Does sleep deprivation, for instance, trigger higher adrenaline levels, encourage carbohydrate cravings or binges, make us less likely to engage in physical activity? Cortisol is elevated; could this be a factor? I know that I am a different person when sleep-deprived: irritable, less clear-thinking, quicker to anger, more critical, and I develop carbohydrate cravings. It's curious that triglycerides increase when sleep excess is present; what might that represent?

Anyway, the data are growing: Sleep is an important facet of health, both for maintaining a bright outlook and to discourage development of low HDL and high triglycerides. Though not specifically examined in this study, we know that low HDL/high triglycerides are, as a rule, associated with the undesirable small LDL particle pattern.

As a practical matter, you may also find sleep and waking from sleep more satisfying and restful if you sleep in increments of 90 minutes, e.g., 7 1/2 hours (rather than 7 or 8 hours). This is because the full cycle of sleep, from phase 1 to REM (rapid-eye movement sleep), requires 90 minutes for completion. That doped feeling that sometimes develops when awaking will disappear if you sleep according to your sleep cycle, which is usually 90 minutes long.

Is normal TSH too high?

4. June 2008 William Davis (30)

There's no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.

But how do we distinguish "normal" thryoid function from "low" thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.

Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called "negative feedback loop:" If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.

An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)

The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid "rules."

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

In this study, over 30,000 Norwegians without known thyroid disease were enrolled. TSH levels and lipid (cholesterol) levels were measured.

In this large and extraordinary observation, increasing TSH levels were associated with increasing levels of LDL cholesterol and triglycerides, and decreasing HDL. At what level of TSH did this relationship start? At TSH levels as low as 1.0!

In other words, there were perturbations in standard lipid measures even with TSH levels ordinarily regarded as "normal," even "perfect."

A subsequent observation from the HUNT Study was even more recently published:

Thyrotropin Levels and Risk of Fatal Coronary Heart Disease: The HUNT Study

Abstract:

Background Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.

Methods In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.

Results During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.

Conclusions Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.

In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

I believe that these findings are enough cause to begin thinking seriously about monitoring thyroid function more seriously to uncover "borderline" TSH increases in the "normal" range. While higher TSH levels predict cardiovascular events, does thyroid replacement at these levels reduce it? Critics will say it's a big leap, but I think that it is worth at least considering.

Stay tuned for a lengthy Special Report followed by a full booklet on these issues on the www.cureality.com website.

Copyright 2008 Wiliam Davis, MD

Talking heads

4. June 2008 William Davis (0)

Tne Philadelphia NBC affiliate's website carried this commentary from a colleague of mine:

Mark from the Lehigh Valley is curious about scans that can detect heart disease.

He asked, "I am in my early 50s. My father had a heart attack in his 40s. I am healthy with no symptoms of heart disease, should I consider a heart scan?"

"Well, Mark, occasionally family history needs to be considered more closely. If your father had coronary disease at a relatively young age at the absence of any known risk factor for heart disease for example diabetes, smoking, obesity, high blood pressure, than your level of risk should be considered more closely," Dr. Kevin Shinal, a cardiologist, said.

"There are a number of studies available to access [sic] your level of risk. One such study is a calcium score. A calcium score is a form of a CAT scan that access [sic] the calcium burden or presence of calcium in your coronary arteries. It assigns you a score and score is translated into a level of cardiovascular risk," Shinal said.

But the doctor warned because Mark doesn't have active symptoms, the scan probably wouldn't be covered by insurance.

Was there an understandable answer in there? I certainly couldn't find it.

Why pick on some yokel responding inarticulately to the local media's quest for content? Because this is, all too often, what the public hears: Ill-informed blather from someone who has little or no understanding of the issues. Maybe this doctor wanted his practice group to get some free publicity. "Doctor, could you just answer a few questions from viewers?"

Unfortunately, it's not just local media who are guilty of consulting with know-nothings with only passing knowledge of an issue. National media are guilty of it, too. The need to fill airtime with content is better filled with talking heads who present a compelling story, whether or not it is accurate or insightful, rather than an expert with deep insight into a topic who might not present as pretty a story. I've seen this countless times. A good portion of my day, in fact, is occupied responding to patient questions based on the misinformation presented in some media report.

My message of this brief rant: Be very careful of the messages delivered by the media, even if provided by some supposed "expert." In fact, I regard "experts" in health about as believable as politicians. Sure, sometimes they provide accurate information. But they often do not, or provide information with limited understanding. Or, worse, information intended to serve some hidden agenda.

Were the media to ask me to respond to the question, however, I would say:

"Yes, you should absolutely have a heart scan--yesterday! With your family history, there is no other way to accurately, easily, and inexpensively quantify the amount of coronary atherosclerosis in your heart's arteries. A stress test only uncovers advanced disease. A heart catheterization is overkill and absolutely not indicated in an asymptomatic man. Judging the presence of heart disease from cholesterol values is folly.

"What's left? A CT heart scan. So, yes, you need a CT heart scan ASAP with no doubt whatsoever."

But they didn't ask.

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