Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

How to have a heart attack in 10 easy steps

If you would like to plan a heart attack in your future, here are some easy-to-follow steps to get you there in just a few short months or years:


1) Follow a low-fat diet.

2) Replace fat calories with "healthy whole grains" like whole wheat bread.

3) Eat "heart healthy" foods like heart healthy yogurt and breakfast cereals from the grocery store.

4) Use cholesterol-reducing plant sterols.

5) Take a multivitamin to obtain all the "necessary" nutrients.

6) Take the advice of your doctor who declares your heart "in great shape" based on your cholesterol values.

7) Take the advice of your cardiologist who declares your heart "like that of a 30-year old" based on a stress test.

8) Take a statin drug to reduce LDL and c-reactive protein while maintaining your low-fat diet.

9) Neglect sun exposure and vitamin D restoration.

10) Limit your salt intake while not supplementing iodine.



There you have it: An easy, 10-step process to do your part to help your local hospital add on its next $40 million heart care center.

If you would instead like to prevent a heart attack in your future, then you should consider not doing any of the above.

Kick inflammation in the butt

C-reactive protein, or CRP, is a protein produced by the liver in response to inflammatory signals its receives. Thus, CRP has emerged as a popular measure to gauge the underlying inflammatory status of your body. Higher CRP levels (e.g., 3.0 mg/L or greater) are associated with increased risk of heart attack and other cardiovascular events.

The drug cartel have jumped on this with the assistance of Harvard cardiologist, Dr. Paul Ridker. Most physicians now regard increased CRP as a mandate to institute statin therapy, preferably at high doses based on such studies as The JUPITER Trial, in which rosuvastatin (Crestor), 20 mg per day, reduced CRP 37%.

I see this differently. Two strategies drop CRP dramatically, nearly to zero with rare exception: Vitamin D restoration and wheat elimination. Not 37%, but something close to 100%.

Yes, I know it sounds wacky. But it works almost without fail, provided the rest of your life is conducted in reasonably healthy fashion, i.e., you don't live on Coca Cola, weigh 80 lbs over ideal weight, and smoke.

How can something so easily reduced like CRP mean you "need" medication? Easy: Increased CRP means there are fundamental deficiencies and/or inflammation provoking foods in your diet. Correct neither and there is an apparent benefit to taking a statin drug.

Why not just correct the underlying causes?

Life without Lipitor

One of the most common reasons people come to my office is to correct high cholesterol values without Lipitor. (Substitute "Lipitor" with Crestor, simvastatin, Vytorin, or any of the other cholesterol drugs; it's much the same.)

In the world of conventional healthcare, in which you are instructed to follow a diet that increases risk for heart disease and not advised to correct nutrient deficiencies like vitamin D and omega-3 fatty acids, then a drug like Lipitor may indeed provide benefit.

But when you are provided genuinely effective information on diet, along with correction of nutrient deficiencies, then the "need" and apparent benefits of Lipitor largely dissolve. While there are occasional genetic anomalies that can improve with use of Lipitor and other statins, many, perhaps most, people taking these drugs really would not have to if they were just provided the right information.

Anyone following the discussions on these pages knows that wheat elimination is probably one of the most powerful overall health strategies available. Wheat elimination reduces real measured LDL quite dramatically. Provided you limit other carbohydrates, such as those from fruits, as well, LDL can drop like a stone. That's not what your doctor tells you. This approach works because elimination of wheat and limiting other carbohydrates reduces small LDL. Small LDL particles are triggered by carbohydrates, especially wheat; reducing carbohydrates reduces small LDL. Conventional LDL of the sort obtained in your doctor's office will not show this, since it is a calculated value that appears to increase with reduced carbohydrates, a misleading result.

Throw vitamin D normalization and iodine + thyroid normalization into the mix (both are exceptionally common), and you have two additional potent means to reduce (measured) LDL. Not restricting fat but increasing healthy fat intake, such as the fats in lots of raw nuts, olive oil, and flaxseed oil reduce LDL.

While I still prescribe statins now and then, a growing number of people are succeeding without them.

(Note that by "measured" LDL I am referring to the "gold standard," LDL particle number by NMR provided by Liposcience. A second best is measured Apoprotein B available through most conventional labs.)

In search of wheat: Emmer

While einkorn is a 14-chromosome ancient wheat (containing the so-called "A" genome), emmer is a 28-chromosome wheat (containing the "A" and "B" genomes, the "B" likely contributed by goat grass 9000 years ago).

Both einkorn and emmer originally grew wild in the Fertile Crescent, allowing Neolithic Natufians to harvest the wild grasses with stone sickles and grind the seeds into porridge.

Having tested einkorn with only a modest rise in blood sugar but without the gastrointestinal or neurological effects I experienced with conventional whole wheat bread, I next tested bread made with emmer grain.

The emmer grain was ground just like the other two grains, cardiac dietitian Margaret Pfeiffer doing all the work of grinding and baking. Margaret added nothing but water, yeast, and a little salt. The emmer rose a little more than einkorn, but not to the degree of conventional whole wheat.

I tested my blood sugar beforehand: 89 mg/dl. I then ate 4 oz of the emmer bread. It tasted very similar to conventional whole wheat, but not as nutty as einkorn. Also not as heavy as einkorn, only slightly heavier than conventional whole wheat.

One hour later, blood sugar: 147 mg/dl. I felt slightly queasy for about 2-3 hours, but that was the end of it. No abdominal cramps, no sleep disturbance or crazy dreams, no nausea, no change in ability to concentrate.

I asked four other wheat-sensitive people to try the emmer bread. Likewise, nobody reacted negatively (though nobody tested blood sugar).

So it seems to me, based on this small, unscientific experience, that ancient einkorn (A) and emmer (AB) wheat seem to act like carbohydrates, similar to, say, rice or quinoa, but lack many of the other adverse effects induced by conventional wheat.

Modern wheat , Triticum aestivum, contains variations on the "A," "B," and "D" genomes, the "D" contributed by hybridization with Triticum tauschii at about the same time that emmer wheat hybridization occurred. It is likely that proteins coded by the "D" genome are the source of most of the problems with wheat products: immune, neurologic, gastrointestinal destruction, airway inflammation (asthma), increase in appetite, etc. This is consistent with observations made in studies that attempt to pinpoint the gliadin proteins that trigger celiac, the area in which much of this research originates.

If I ever would like an indulgence of cookies or cupcakes, I think that I will order some more einkorn grain from Eli Rogosa.

In search of wheat: Another einkorn experience

Lisa is a trained dietitian. Unlike many of her colleagues, she has "seen the light" and realized that the conventional advice that most dietitians are forced to dispense through hospitals, clinics, and other facilities is just plain wrong. 

I know Lisa personally and we've had some great conversations on diet and nutritional supplements. I told Lisa about my einkorn experience and how I witnessed a dramatic difference between bread made from einkorn wheat and that made from conventional whole wheat. So she decided to give it a try herself. 

Here's Lisa's experience:


This past Friday, June 18th, I conducted my "Einkorn Wheat Experiment".

7 am 
FBG [fasting blood glucose] 97 mg/dl

8 am-9 am 
1 hour high-intensity aerobic workout

10:05 am 
BG 99

10:05 am 
I embarked upon the journey of choking down, I mean enjoying, the hefty piece of Einkorn bread. Wow, was that bread dense!  It was a lot of work chewing. 

10:50 am 
(45 minutes after consumption, wanted to see what BG did a bit before the 1 hr mark)  BG 153

11:05 am 
1hr PP 120

11:35 am 
90 mins PP [postprandial] 113

12:05 pm 
2 hours PP  114 ... at this time I ate an egg & veggie omelet for lunch.

12:50 pm 
BG 100

Before dinner 5:10 pm 
BG 88

I was surprised with the BG of 153. However, it was good to see my insulin response is reactive and decreased BG 33 points in 15 minutes to end up with a BG of 120 1 hr after the bread.  

So, it appears my response is similar. A slight elevation of BG at the 1 hour mark, but not to the degree of conventional whole grain wheat bread.  

Of note, also, was the fact that I cannot remember the last time I ate a piece of wheat bread of this magnitude that did not make me bloated... not at all: No cramps, no brain fog, no headache and, did I mention not bloated?  

I believe you are on to something with tolerance of Einkorn wheat for those of us with wheat sensitivities, in addition to its apparent lower glycemic response.

Along with Lisa, I asked four other people with various acute intolerances (all gastrointestinal) to conventional wheat, i.e., people who experience undesirable effects from wheat within minutes to several hours, to eat the einkorn bread. None experienced their usual reactions.

Obviously, this does not constitute a clinical trial. Nonetheless, I find this a compelling observation: People like myself who generally experience distinct undesirable reactions to wheat did not experience these reactions with einkorn.

Note, however, that einkorn behaves like a carbohydrate. No different, say, from brown rice or quinoa. However, unlike modern whole wheat flour from Triticum aestivum,  in this little experience there were no immune reactions, no neurologic phenomena, no gastrointestinal distress--just the blood sugar consequences.

While this may not be true for all people consuming einkorn, it suggests that primordial einkorn wheat is quite different from modern conventional wheat for most people.

Increased blood calcium and vitamin D

Conventional advice tells us to supplement calcium, 1200 mg per day, to preserve bone health and reduce blood pressure.

Here's a curious observation I've now witnessed a number of times: Some people who supplement this dose of calcium while also supplementing vitamin D sufficient to increase 25-hydroxy vitamin D blood levels to 60-70 ng/ml develop abnormally high levels of blood calcium, hypercalcemia.

This makes sense when you realize that intestinal absorption of calcium doubles or quadruples when vitamin D approaches desirable levels. Full restoration of vitamin D therefore causes a large quantity of calcium to be absorbed, more than you may need. In addition, two studies from New Zealand suggest that 1200-1300 mg calcium with vitamin D per day doubles heart attack risk.

We have 20 years of clinical studies demonstrating the very small benefits of supplementing calcium to stop or slow the deterioration of bone density (osteopenia, osteoporosis). These studies were performed with no vitamin D or with trivial doses, too small to make a difference. I believe those data have been made irrelevant in the modern age in which we "normalize" vitamin D.

Should hypercalcemia develop, it is not good for you. Over long periods of time, abnormal calcium deposition can occur, leading to kidney stones, atherosclerosis, and arthritis.

Until we have clarification on this issue, I have been advising patients to take no more than 600 mg calcium supplements per day. I suspect, however, that the vast majority of us require no calcium at all, provided an overall healthy diet is followed, especially one that does not leach out bone calcium. This means no foods like those made with wheat or containing powerful acids, such as those in carbonated drinks.

Heart health consultation with Dr. Joe D. Goldstrich

Cardiologist, nutritionist, and lipidologist, Dr. Joe D. Goldstrich, is a frequent contributor to the Track Your Plaque Forum, where we discuss the full range of issues relevant to coronary health and coronary plaque reversal.

I have come to value Dr. Goldstrich's unique insights, especially in nutrition. Formerly National Director of Education and Community Programs for the American Heart Association and a physician at the Pritikin Center, his dietary philosophy has evolved away from low-fat and towards a low-carbohydrate focus, much as we use in Track Your Plaque. Like TYP, Dr. Goldstrich is always searching for better answers to gain control over coronary health. His unique blend of ideas and background has helped us craft new ideas and strategies. Dr. Goldstrich has proven especially adept at understanding how to incorporate new findings from clinical studies in our framework of coronary atherosclerotic plaque management strategies.

Dr. Goldstrich is offering to share his expertise with our online community. If you would like a one-on-one phone consultation with Dr. Goldstrich, you can arrange to speak with him at his HealthyHeartConsultant.com website.

Wheat aftermath

Following my 4 oz whole wheat misadventure that yielded the sky-high blood sugar of 167 mg/dl, compared to einkorn wheat's 110 mg/dl, I suffered through a 36-hour period of misery.

After I obtained the blood sugar of 167 mg/dl, I biked hard for one hour. This yielded a blood sugar back down in the 80s. I felt spacey in the ensuing few hours, as well as a little queasy. However, about 12 hours later, I awoke with overwhelming nausea along with that hypersalivating thing that happens just prior to vomiting. It did not come to that, but persisted all through the following day.

The next morning, I could barely concentrate. Trying to read a study (admittedly on the complex topic of agricultural genetics), I had to read each paragraph 4 or 5 times. Abdominal cramps and a bloated feeling also developed, though I was able to eat.

The 2nd night was filled with incredibly vivid dreams and intermittent sleeplessless. I awoke about 5 times through the night, but periods of sleep were filled with detailed, colorful dreams. I dreamt that a large corporation was secretly trying to gain control over the world's water supply, and I snuck onto a complex underwater vessel that was exploring and mapping the coastline of the Great Lakes in preparation. Weird.

I recognized these odd feelings as various facets of wheat intolerance, since they were all reminiscent of feelings I used to experience before I removed wheat from my diet. They were amplified and compressed, likely because I had been wheat-free for so long.

The odd thing is that, despite the modest blood sugar effect of my einkorn experience, none of the gastrointestinal or neurologic effects of wheat developed. So far, two other people with acute gastrointestinal wheat sensitivities have consumed our einkorn bread, also without reproduction of their usual symptoms.

Einkorn contains gluten, though the structure of the many gluten proteins of einkorn differs from that of the wheat bread I consumed, an example of modern Triticum aestivum. 14-chromosome einkorn carries what biologists call the "A" genome, while Triticum aestivum has the combines genomes of 3 plants, the combination of the A, B, and D genomes. It is the D genome that contains the genes coding for the most obnoxious, immunogenic forms of gluten.

So einkorn may not be entirely benign, but it is a good deal less obnoxious than modern Triticum aestivum.

I am awaiting the reports from a few other people on their experiences.

In search of wheat: Einkorn and blood sugar

There are three basic aspects of wheat's adverse health effects: immune activation (e.g., celiac disease), neurologic implications (e.g., schizophrenia and ADHD), and blood sugar effects.

Among the questions I'd like answered is whether ancient wheat, such as the einkorn grain I obtained from Eli Rogosa, triggers blood sugar like modern wheat.

So I conducted a simple experiment on myself. On an empty stomach, I ate 4 oz of einkorn bread. On another occasion I ate 4 oz of bread that dietitian, Margaret Pfeiffer, made with whole wheat flour bought at the grocery store. Both flours were finely ground and nothing was added beyond water, yeast, olive oil, and a touch of salt.

Here's what happened:

Einkorn wheat bread:

Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 110 mg/dl

Conventional wheat bread
Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 167 mg/dl

The difference shocked me. I expected a difference between the two, but not that much.

After the conventional wheat, I also felt weird: a little queasy, some acid in the back of my throat, a little spacey. I biked for an hour solid to reduce my blood sugar back to its starting level.

I'm awaiting the experiences of others, but I'm tantalized by the possibility that, while einkorn is still a source of carbohydrates, perhaps it is one of an entirely different variety than modern Triticum aestivum wheat. The striking difference in blood sugar effects make me wonder if einkorn eaten in small quantities can keep us below the Advanced Glycation End-Product threshold.
 

No more Lovaza

That's it: I will NEVER ever write another prescription for Lovaza.

I actually very rarely write a prescription for Lovaza, i.e., prescription fish oil. But this was the last straw.

I advised a patient that we've had good success using high-doses of fish oil to reduce lipoprotein(a), Lp(a). 6000 mg per day of the omega-3 component (EPA + DHA) from fish oil reduces Lp(a) in 60% of people after one year. (Recall that Lp(a) is the most aggressive known lipid-related cause of heart disease.)

The two preparations I generally suggest are either the very affordable Sam's Club Members Mark Triple-Strength Fish Oil with 900 mg EPA + DHA per capsule: 7 capsules per day. Another great product (my personal favorite because of its extreme purity--it doesn't even smell like fish oil): Pharmax Finest Pure Fish Oil with 1800 mg EPA + DHA per teaspoon: 3 to 3 1/2 teaspoons per day.

Both preparations work great and are quite affordable, given the high dose. For the Sam's Club preparation, it will cost around $30 per month, while the Pharmax liquid will run around $49 per month.

Well, the woman's husband insisted on a prescription for Lovaza. One Lovaza capsule contains 784 mg EPA + DHA per capsule: 7 to 8 capsules per day.

Here are some prices for Lovaza from online pharmacy discounters:
Prescription Giant: $78.99 for 30 capsules ($2.63 per capsule)
Planet Drugs Direct: $135 for 100 capsules ($1.35 per capsule)

These are lower than the prices I obtained in past by calling local pharmacies in my area, quite a bit lower, in fact.

Filling the Lovaza prescription at Prescription Giant will therefore cost $552.93 to $631.92 per month; at Planet Drugs Direct it will cost $283.50 to $324.00 per month. At local pharmacies, a similar 7 to 9 capsules Lovaza per day will cost upwards of $800 to $900 per month.

The patient's husband insisted on the Lovaza prescription because he knew that his insurance would cover it. When I pointed out that this was a large cost that would have to be borne by others in their healthcare premiums, he said that didn't matter to him.

I hesitated, but ended up writing the prescription for 7 Lovaza capsules per day. As soon as I handed to him, I regretted it. In fact, I am embarassed and angry at myself for having given in.

So I vowed: I will NEVER EVER write another prescription for Lovaza.

I do not believe that we should spread the excessive profiteering of the pharmaceutical industry around on the backs of people who pay their healthcare insurance premiums, just so that a few people, like this selfish couple, can save a few dollars a month.

This is your brain on wheat II

In the original Heart Scan Blog post, This is your brain on wheat, I discussed how opioid peptides (i.e., small proteins that act like opiates such as heroine or morphine) that result from digestion of wheat cause unique effects on the human brain, particularly addictive behaviors. I also briefly reviewed how elimination of wheat has been shown to reduce auditory hallucinations and other psychotic behaviors in a subset of people with paranoid schizophrenia.

These two phenomena, addictions and schizophrenia, are most likely the result of exorphins that cross the blood-brain barrier. Exorphins--exogenous morphine-like compounds--can be blocked by opiate-blocking drugs like naloxone and naltrexone. Naloxone is used in hospitals to reverse morphine or heroine overdoses; naltrexone is being repackaged into a weight loss drug, since blocking wheat-derived exorphins reduces appetite. (Yes: The USDA tells us to eat more wheat, the drug industry sells us the antidote.)

There's another way that wheat can affect the brain and nervous system: immune-activated damage.

This is similar to the effect seen in celiac. There's even overlap with some of the antibody markers used to diagnose celiac, like the anti-gliadin antibodies and the anti-endomysium antibodies.

The most common immune neurological syndrome consequent to wheat consumption is cerebellar ataxia, a condition in which an immune response causes damage to the Purkinje cells of the cerebellum, the portion of the brain responsible for balance and coordination. This results in stumbling, incoordination, incontinence, and eventually leads to reliance on a cane or walker and wearing a diaper. Average age of onset: 53 years. A shrunken, atrophied cerebellum can be seen on an MRI of the brain.

Problem: Most people with central nervous system damage caused by wheat do not have any intestinal symptoms, like diarrhea and abdominal pain, the sort of symptoms usually associated with celiac disease. It means the first sign of wheat-induced brain damage may be bumping into walls and wetting your pants.

There's no such thing as a "no-carb" diet

When I tell patients how I advise a wheat-free, cornstarch-free, sugar-free diet on the background of a low-carbohydrate diet, some people ask: "But can I live on a no-carb diet?"

Well, there's no such thing as a "no-carb" diet. Low-carb, yes. No-carb, no.

Here are the carbohydrate contents of various "low-carb" foods:

Gouda cheese--3 oz contains 1.65 grams carbohydrates
Mozzarella cheese--1 cup contains 2.89 grams carbohydrates
Walnuts--4 oz (56 nuts) contains 2.96 grams carbohydrates
Almonds--4 oz contains 1.38 grams carbohydrates
Sour cream--one-half cup contains 3.31 grams carbohydrates
Red wine--3.5 oz glass contains 2.69 grams carbohydrates
Eggplant--1 cup cooked contains 8.33 grams carbohydrates
Green pepper--1 medium-sized raw contains 5.52 grams carbohydrates
Cucumber--1 medium contains 4.34 grams carbohydrates
Tomato--1 medium contains 4.82 grams carbohydrates

(Nutrition data from USDA Nutrient Database)

In other words, foods thought to be "low-carb" actually contain a modest quantity of carbohydrates.

Such modest quantities of carbohydrates may not be enough to trip your blood sugar. But add up all the "low-carb" foods you consume over the course of a day and you can easily achieve 30 grams or more carbohydrates per day even without consuming any higher carbohydrate foods.

Why doesn't your doctor try to CURE diabetes?

Imagine you have breast cancer. You go to your doctor and she says, "As your pain worsens, we'll help you with pain medication. We'll fit you with a special bra to accommodate the tumor as it grows. That's all we're going to do."

"What?" you ask. "You mean just deal with the disease and its complications, but you're not going to help me get rid of it . . . cure it?"

It would be incredibly shocking to receive such advice. Then why is that the sort of advice given when you are diagnosed with diabetes?

Say you go to the doctor. Lab values show a fasting blood sugar of 156 mg/dl, HbA1c (a reflection of your previous 60 days average glucose) of 7.1%. Both values show clear-cut diabetes.

Your doctor advises you to 1) start the drug metformin, then 2) talk to the diabetic teaching nurse or dietitian about an American Diabetes Association (ADA) diet.

The ADA diet prescribed encourages you to increase carbohydrates and cut fats at each meal and maintain a consistent intake so that you don't experience hypoglycemic (low blood sugar) episodes. You follow the diet, which causes you to gain 10-15 lbs per year, increasing your "need" for diabetes medication. You doctor adds Actos, then Januvia, then injections of Byetta.

Three years and 34 lbs later, you are not responding well to the drug combination with blood sugars rarely staying below 200 mg/dl. You've developed protein in your urine ("proteinuria"), lost 30% of your kidney function, and you are starting to lose sensation in your feet. So the doctor replaces some of your medication with several insulin injections per day.

This formula is followed millions of times per year in the U.S. So where along the way did your doctor mention anything about a "cure"?

Adult diabetes is the one chronic disease that nobody cares to cure. Treat it, maintain control over blood sugars, but cure it? Most physicians say it's impossible.

The tragedy is that diabetes is a curable condition. I've seen it happen many times. Physicians dedicated to curing diabetes like low-carb expert, Dr. Mary Vernon, have cured it countless times. Dr. Eric Westman and colleagues have been building the case for the carbohydrate-restricted cure for diabetes with studies such as this. In this last study, of the 8 participants on insulin + medications at the start of the study, 5 no longer required medications at the close of the study--they were essentially non-diabetic.

I tell patients that diabetes, in fact, is a disease you choose to have or not to have--provided you are provided the right diet and tools. Sadly, rarely are diabetics told about the right diet and tools.

That's why Cadbury Schweppes has been a major contributor to the American Diabetes Association, as are other processed food manufacturers and the drug industry, all who stand to profit from maintaining the status quo.

The cure? Eliminate or at least dramatically reduce carbohydrates, the foods that increase blood sugar.

Note: If you have diabetes and you are taking any prescription agents, such as glyburide, glipizide, insulin, and some others, you will need to discuss how to manage your medications if you reduce carbohydrates. The problem is finding a doctor or other resource to help you do this.

LDL pattern B

Here's a Q&A I stumbled on in the Forum of MedHelp, where people obtain answers from presumed health "experts."

Question:

My VAP test results in July 07 identified an LDL Pattern B.
Overall results:
Total 150
HDL 75
LDL 61
Trig 60
HDL-2 17
LP(a) 6.0
LDL Pattern B

Medications:
Lipitor 10mg
Zetia 10mg
Altace 10mg
Atenolol 50mg
Plavix 75mg
Aspirin 81mg

I had several heart attacks which resulted in CABG performed May 2000. I am a 53 year old white male , 6'1", 190 pounds, exercise every day, watch my diet and feel great. Everything looks OK except my LDL Pattern B. Is there any therapy to improve the Patten B?


Answer from CCF, MD:
Your results indicate an LDL pattern B, which generally indicates small atherogenic LDL particles which may cause increased risk for CAD. However, there are several problems with LDL patterning: 1) its unreliability (of LDL pattern testing ), 2) unclear clinical evidence regarding regarding the usefulness of LDL patterns and particle size. The majority of evidence regarding the progression of atherosclerosis is with LDL lowering and to an smaller extent HDL raising.

All available clinical evidence shows that any particles in the VLDL, IDL, or LDL range are atherogenic, and there is no evidence that whether belonging to pattern A or B one is more atherogenic than others.

Subclass studies have proliferated over the last few years, but many of these studies were funded or subsidized either by suppliers of the assays as a method to expand their use and move them into mainstream practice, or by pharmaceutical companies in an attempt to claim some advantage over other therapeutic agents.
Thus, current data on LDL subclasses are at best incomplete and at worst misleading, suffering from publication bias, and now given the recent results of the Ensign et al. study, unreliable.

Your LDL, and HDL are at goal. The Lpa level is still not clearly linked as a modifiable risk factor for CAD, although elevated levels are now know to be linked to stroke.

Continue with your present treatments: aspirin, plavix, ateonol and altace are all essential medications.



Wow. The extent of ignorance that pervades the ranks of my colleagues is frightening.

Contrary to the response, LDL particle size assays are quite reliable and accurate. I've performed many thousands of lipoprotein assays and they yield reproducible and clinically believable results. For example, eliminate wheat, oats, cornstarch, and sugars and small LDL drops from 2400 nmol/L to 893 nmol/L (NMR)--huge drops. If repeated within a short period of time, the second measure will correspond quite closely.

The data are also quite clear: Small LDL particles (i.e., "pattern B") are a potent predictor of cardiovascular events. What we lack are the treatment trials that show that reduction of small LDL results in reduced cardiovascular events. The reason for this is that small LDL research is not well-funded, since there is no prescription drug to treat small LDL, only nutritional means. Niacin (as Niaspan) is as close as it comes for a "drug" to reduce small LDL. But diet is far more effective.

Given the questioner's fairly favorable BMI of 25.1 and his history of aggressive heart disease, it is virtually certain that he has what I call "genetic small LDL," i.e., small LDL that occur on a genetically-determined basis (likely due to variants of the cholesteryl-ester transfer protein, or CETP, or of hepatic lipase and others).

Ignoring this man's small LDL will, without a doubt, consign him to a future of more heart attacks, stents, and bypass. Maybe by that time the data supporting the treatment of small LDL will become available.

What increases blood sugar more than wheat?

Take a look at these glycemic indexes (GI):


White bread 69
Whole wheat bread 72
Sucrose 59
Mars bar 68
White rice 72
Brown rice 66


I've made issue in past of whole wheat's high GI--higher than white bread. Roughly in the same glycemic league as bread are shredded wheat cereal, brown rice, and a Mars candy bar.

With few exceptions, wheat products have among the highest GIs compared to the majority of other foods. For instance:


Kidney beans 29
Chick peas 36
Apple 39
Ice cream 36
Snickers Bar 40


Yes, by the crazy logic of glycemic index, Snickers is a low-glycemic index food.

While I do not believe that low GI makes a food good or desirable, since low GI foods still provoke high blood sugars, small LDL particles, trigger glycation, and other abnormal phenomena, they are clearly less obnoxious than the items in the first list.

Take a look at this list:

Cornflakes 80
Rice cakes 80
Rice Krispies 82
Rice pasta, 92
Instant potatoes 83
Tapioca 81



Starches that are dried and/or pulverized, such as cornstarch, potato starch, rice starch, and tapioca starch (cassava root) will increase blood sugar even more than wheat. Foods with these starches have GI's of 80-100.

Cornstarch, potato starch, rice starch, and tapioca starch: Sound familiar? These are the main starches used in "gluten-free" foods. A hint of the high GI behavior of these dried starches is seen in the GI for cornflakes of 80.

So remember: Wheat-free is not the same as gluten-free. Gluten-free identifies junk carbohydrates masquerading as healthy because they don't contain one unhealthy ingredient, i.e. wheat.

China fiction?

Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk.

Richard Nikoley of Free the Animal and Stephan Guyenet of Whole Health Source have been talking about an analysis of the China Study raw data performed by a young woman named Denise Minger.

Denise's analysis is nothing short of brilliant, absolutely "must" reading for anyone interested in nutrition.

Her comments on the relationship of wheat to heart disease:

Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?

Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease?

Carbohydrate-LDL double whammy

Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.

The list of reasons why small LDL particles are more atherogenic, i.e., plaque-causing, is long:

--Small LDL particles, being smaller, more readily penetrate the endothelial barrier of the arterial wall.
--Small LDL particles are more adherent to glycosaminoglycans in the artery wall.
--Small LDL particles are poorly taken up by the liver LDL receptor, but enthusiastically taken up by macrophage receptors of the sort in your artery walls.
--Because of their poor liver clearance, small LDL persists in the bloodstream far longer than large LDL.
--Small LDL particles are more oxidation-prone. Oxidized LDL are more likely to trigger inflammatory phenomena and be taken up by macrophages in the artery wall.

Let me add another reason why small LDL particles are more likely to cause plaque: They are more likely to undergo glycation. (More on glycation here.)

Glycation occurs when glucose (sugar) molecules in the blood or tissue modify proteins, usually irreversibly. Small LDL particles are uniquely glycation-prone. (This is likely due to a conformational change of the apoprotein B in the small LDL particle, exposing lysine residues along apo B that become glycated.)

Here's a great demonstration of this phenomenon by Younis et al:


"LDL3" is the small type. Note that small LDL particles are 4-5 times more glycated than large LDL. That's a big difference.

Once glycated, small LDL is especially resistant to being taken up by the liver. Like annoying in-laws, they hang around and hang around and . . . The longer they hang around, they more opportunity they have to contribute to plaque formation.

So, carbohydrates trigger formation of small LDL particles. Once formed, small LDL particles are glycated when blood sugar increases. While LDL can be glycated even when blood sugars are in the normal range (90 mg/dl or less), glycation goes berserk when blood sugars go higher, such as a blood sugar of 155 mg/dl after a bowl of steel-cut oatmeal.

To lose weight, prick your finger

We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day.

So how can you stop triggering insulin?

The easiest way is to eliminate, or at least minimize, carbohydrates. My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket.

Another way is to check your blood sugar one hour after completing a meal and keep your after-eating, or "postprandial," blood sugar 100 mg/dl or less. Let's say you are going to eat stone ground oatmeal, for example. Blood sugar prior to eating is, say, 90 mg/dl. One hour after oatmeal it's 168 mg/dl--you know that this is going to trigger insulin and make you fat. Oatmeal should therefore be eliminated.

Keeping blood sugar to 100 mg/dl or less after eating teaches you how to avoid provocation of insulin. A shrinking tummy will follow.

To do this, you will need:

1) A glucose meter--My favorite is the One Touch Ultra Mini ($13.42 at Walmart). It's exceptionally easy to use and requires just a dot of blood. Drawback: Test strips are about $1 each. Accuchek Aviva is another good device. (We've had a lot of problems with Walgreen's brand device.)
2) Test strips--This is the costly part of the proposition. Purchased 25 or 50 at a time, they can cost from $0.50 to $1.00 a piece.
3) Lancets--These are the pins for the fingerstick device that comes with the glucose meter. A box should be just a few dollars.

No prescription is necessary, nor will insurance pay for your costs unless you're diabetic. To conserve test strips, use them only when a new, untested food or food combination is going to be consumed. If you had two scrambled eggs with green peppers, sundried tomatoes, and olive oil yesterday and had a one hour postprandial glucose of 97 mg/dl, no need to check blood sugar again if you are having the same meal again today.

Iodine update

As the iodine experience grows, I've made several unique observations.

Up to several times per day, I see people who are responding in some positive way to iodine supplementation. (See previous Heart Scan Blog posts about iodine: Iodine deficiency is REAL and The healthiest people are the most iodine deficient.)

Among the phenomena I've observed:

1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development.

2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.

3) Reversal of small goiters also occurs over about 6 months.

4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months.

5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet.

6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures.

7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L.


Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females.

All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.

Quieting the insulin storm

The cycle of eating, satiety, and hunger is largely driven by insulin and blood sugar responses.

For instance, if I eat a bowl of Cheerios, my blood sugar will surge to 140 mg/dl or higher (how high depending on insulin sensitivity). The flood of sugar from this Frankenfood triggers the release of insulin; blood sugar then settles back down.

The decline in blood sugar back down to normal or below normal powerfully triggers hunger. Variable degrees of shakiness, mental fogginess, and irritability also commonly occur. Most people experience this to some extent; some experience an exagerrated version called "reactive hypoglycemmia" and can suffer peculiar personality changes, irrational and even violent behavior.

Foods made with wheat or cornstarch raise blood sugar higher and faster than table sugar. Accordingly, blood sugar and insulin swing more widely with these food: highs are higher, lows are lower. People who therefore follow the standard mantra of "eat plenty of healthy whole grains" therefore experience a 2-3 hour long cycle of eating, brief satiety, and recurrent hunger. Cravings for snacks, impulsive eating, and overeating all occur during the period when blood sugar has dropped and hunger is powerfully triggered.

Eliminating this up and down fluctuation is therefore key to regaining control over appetite, losing weight, reducing small LDL and triglycerides, reducing blood sugar, and putting out the fires of inflammatory responses.

You can accomplish this by:

1) Eliminating foods that trigger the exagerrated rises in blood sugar--Wheat, cornstarch, polished rices, white and red potatoes, and candy.

2) Adding a healthy oil to every meal--a strategy that prolongs satiety and helps suppress sugar-insulin fluctuations.


The ful nuts and bolts details of this diet will be released with the New Track Your Plaque Diet. Part I has already been released; part II is coming any day on the Track Your Plaque website.

Scare tactics

I've seen this happen many times. Despite the great media exposure and the growing acceptance of my colleagues, heart scans still trigger wrong advice. I had another example in the office today.

Henry got a CT heart scan in 2004. His score: 574. In his mid-50s, this placed him in the 90th percentile, with a heart attack risk of 4% per year. Henry was advised to see a cardiologist.

The cardiologist advised Henry, "Oh, that's just a 'false positive'. It's not true. You don't have any heart disease. Sometimes calcium just accumulates on the outside of the arteries and gives you these misleading tests. I wish they'd stop doing them." He then proceeded to advise Henry that he needed a nuclear stress test every two years ($4000 each time, by the way). No attempt was made to question why his heart scan score was high, since the entire process was outright dismissed as nonsense.

I'm still shocked when I hear this, despite having heard these inane responses for the past decade. Of course, Henry's heart scan was not a false positive, it was a completely true positive. I'm grateful that nothing bad happened to Henry through two years of negligence, though his heart scan score is likely around 970, given the expected, untreated rate of increase of 30%.

The cardiologist did a grave disservice to Henry: He misled him due to his ignorance and lack of understanding. I wish Henry had asked the cardiologist whether he had read any of the thousands of studies now available validating CT heart scans. I doubt he's bothered to read more than the title. The cardiologist is lucky (as is Henry) that nothing bad happened in those two years.

Do false positives occur as the cardiologist suggested? They do, but they're very rare. There's a rare phenomenon of "medial calcification" that occurs in smokers and others, but it is quite unusual. >99% of the time, coronary calcium means you have coronary plaque--even if the doctor is too poorly informed to recognize it.

What's better than a heart scan?


Do you know what's better than a heart scan?

Two heart scans. No other method can provide better feedback on the results of your program.

Say you've made efforts to correct high LDL; lost weight to raise HDL and reduce small LDL; added soluble fibers, nuts, and dramatically reduced wheat products; take fish oil, vitamin D, and follow a flavonoid-rich diet. Has it worked?

After a year or so of your program, that's when another heart scan can give you invaluable feedback on whether it's been successful. I tell my patients that it's relatively easy to correct lipid and lipoprotein abnormalities. The difficult part is to know when it's good enough. Is your LDL of 67 mg/dl and HDL of 50 mg/dl good enough? Another heart scan score is the best way I know of to find out.

Variation in plaque growth differs hugely from one person to another, even at equivalent lipoprotein values. Why? Lots of reasons. Humans are inconsistent day to day. Lipoproteins, being a snapshot in time and not a cumulative value, change somewhat from day to day. There's also the possibility of unmeasured, unrecognized factors that influence coronary plaque growth. We may not be smart enough to identify these hidden factors yet. But your heart scan score will incorporate the effects of these hidden factors.

Ideally, we aim for zero growth in plaque (no change in score) or a reduction. But, particularly in the first year, 10% or less plaque growth is still a good result that predicts much reduced risk of heart attack. More than 20% per year and your program needs more work--or else you know what's ahead.

Lipids are snapshots in time; heart scans are cumulative

Let me paint a picture. It's fictional, though a very real portrait of how things truly happen in life.

Michael is an unsuspecting 40-year old man. He hasn't undergone any testing: no heart scan, no lipids or lipoproteins. But we have x-ray vision, and we can see what's going on inside of him. (We can't, of course, but we're just pretending.) Average build, average lifestyle habits, nothing extraordinary about him. His lipids/lipoproteins at age 40:

--LDL cholesterol 150 mg/dl
--HDL cholesterol 38 mg/dl
--Triglycerides 160 mg/dl
--Small LDL 70% of all LDL

At age 40, with this panel, his heart scan score is 100. That's high for a 40-year old male.

Fast forward 10 years. Michael is now 50 years old. Michael prides himself on the fact that, over the past 10 years, he's felt fine, hasn't gained a single pound, and remains as active at 50 as he did in 40. In other words, nothing has changed except that he's 10 years older. His lipids and lipoproteins:

--LDL cholesterol 150 mg/dl
--HDL cholesterol 38 mg/dl
--Triglycerides 160 mg/dl
--Small LDL 70% of all LDL

Some of you might correctly point out that just simple aging can cause some deterioration in lipids and lipoproteins, but we're going to ignore these relatively modest issues for now.)

Lipids and lipoproteins are, therefore, unchanged. Michael's heart scan score: 1380, or an approximate 30% annual increase in score. (Since Michael didn't know about his score, he took no corrective/preventive action.)

My point: If we were to make our judgment about Michael's heart disease risk by looking at lipids or lipoproteins, they would'nt tell us where he stood with regards to heart disease risk. His lipids and lipoproteins were, in fact, the same at age 50 as they were at age 40. That's because measures of risk like this are snapshots in time.

In contrast, the heart scan score reflects the cumulative effects of life and lipids/lipoproteins up until the day you got your scan.

Which measure do you think is a better gauge of heart attack risk? I think the answer's obvious.

The recognition of the metabolic syndrome as a distinct collection of factors that raise heart disease risk has been a great step forward in helping us understand many of the causes behind heart disease.

Curiously, there's not complete agreement on precisely how to define metabolic syndrome. The American Heart Association and the National Heart, Lung, and Blood Institute issued a concensus statement in 2005 that "defined" metabolic syndrome as anyone having any 3 of the 5 following signs:





Waist size 40 inches or greater in men; 35 inches or greater in women

Triglycerides 150 mg/dL or greater (or treatment for high triglycerides)

HDL-C <40 mg/dL in men; <50 mg/dL in women (or treatment for reduced HDL-C)

Blood Pressure >130 mmHg systolic; or >85 mmHg diastolic (or drug treatment for hypertension)

Glucose (fasting) >100 mg/dL (or drug treatment for elevated glucose)


Using this definition, it has become clear that meeting these criteria triple your risk of heart attack.

But can you have the risk of metabolic syndrome even without meeting the criteria? What if your waste size (male) is, 36 inches, not the 40 inches required to meet that criterion; and your triglycerides are 160, but you meet none of the other requirements?

In our experience, you certainly can carry the same risk. Why? The crude criteria developed for the primary practitioner tries to employ pedestrian, everyday measures.

We see people every day who do not meet the criteria of the metabolic syndrome yet have hidden factors that still confer the same risk. This includes small LDL; a lack of healthy large HDL despite a normal total HDL; postprandial IDL; exercise-induced high blood pressure; and inflammation. These are all associated with the metabolic syndrome, too, but they are not part of the standard definition.

I take issue in particular with the waist requirement. This one measure has, in fact, gotten lots of press lately. Some people have even claimed that waist size is the only requirement necessary to diagnose metabolic syndrome.

Our experience is that features of the metabolic syndrome can occur at any waist size, though it increases in likelihood and severity the larger the waist size. I have seen hundreds of instances in which waist size was 32-38 inches in a male, far less than 35 inches in a female, yet small LDL is wildly out of control, IDL is sky high, and C-reactive protein is markedly increased. These people obtain substantial risk from these patterns, though they don't meet the standard definition.

To me, having to meet the waist requirement for recogition of metabolic syndrome is like finally accepting that you have breast cancer when you feel the two-inch mass in your breast--it's too late.

Recognize that the standard definition when you seen it is a crude tool meant for broad consumption. You and I can do far better.

What role DHEA?




DHEA, the adrenal gland hormone, has suffered its share of ups and downs over the years.

Initially, DHEA was held up as the fountain of youth with hopes of turning back the clock 20 years. Such extravagant dreams have not held up. But DHEA can still be helpful for your program.

All of us had oodles of DHEA in our bodies when we were in our 20s and 30s. Gradually diminishing levels usually reach nearly blood levels of around zero by age 70.



In our heart disease prevention program, of course, we aim to stop or reduce your CT heart scan score. Does DHEA reduce your score? No, it most certainly does not. But it can be helpful for gaining control over some of the causes behind coronary plaque.

For instance, DHEA can:

--Help reduce abdominal fat and increase muscle mass (slightly)
--Provide more physical stamina.
--Boost mood.
--It may modestly reduce some of the phenomena associated with the metabolic syndrome (high blood pressure, high blood sugar, high insulin, low HDL, small LDL, etc.)

In my experience, people who feel better do better on their overall program. If you're always tired and run down and run out of steam by 3 pm, I won't see you riding your bicycle outdoors or at the aerobics class. But if you're bursting with energy until you put your head on the pillow, you're more inclined to walk, bike, dance, play with the kids, dance, take Tai Chi, etc.

Some downsides to DHEA: Some people experience aggression. Backing off on the dose usually relieves it. Also, sleeplessness. Taking your DHEA in the morning usually fixes it.



The dose is best tailored to your age and blood levels. People less thaws and other hospitals like it. If you enter the system through your primary care physician or cardiologist, there’s an excellent chance you’ll end up with several procedures, diagnostic and therapeutic, over the ensuing years. Accordingly, St. Matthews provides a very attentive after-discharge follow-up program, complete with access to friendly people, phone centers, “support groups,” and even an occasional festive get-together, all in an effort to ensure future return to the system.

All in all, the St. Matthews Hospital System is a hugely successful operation. It provides jobs for thousands of area residents and provides high-tech, high-quality healthcare. Like any business—and no doubt about it, St. Matthews is a business with all the trappings of a profit-seeking enterprise—it grows to serve its own interests. The tobacco industry didn’t grow to its gargantuan proportions by doing good, but by selling a product to an unsuspecting public. So, too, hospitals.

Curiously, hospitals like St. Matthews continue to operate under the sheltered guise of not-for-profit institution with the associated tax benefits, ostensibly serving the public good. This means that all end-of-year excess revenues are re-invested and not distributed to investors. But non-profit does not mean that individuals within the system can’t benefit, and benefit handsomely. Under St. Matthews’ non-profit umbrella, many businesses thrive: 35 pharmacies, extended care facilities to provide care after hospital discharge, drug and medical device distributors, even a venture capital arm to fund new operations. The financial advantage conferred by “non-profit” status has permitted the hospital to compete with other, for-profit businesses, at a considerable advantage. For this reason, attempts have been made over the years to strip them of what some believe is an unfair advantage; all have failed.

While profits may not fall to the bottom line, money does indeed get paid out to many people along the way. Executives, for instance, pay themselves generous salaries and consulting fees, often from several of the entities in this complex business empire. Physicians are brought in as “consultants” or are awarded “directorships” for hundreds of thousands of dollars per year—Director of Research, Director of Cardiovascular Services, etc. Don’t forget the $3.7 million dollar annual salary paid to the CEO.

Hospitals and doctors have a vested interest in preserving this financial house of cards. They will fiercely battle anyone or anything that threatens the stream of cash. During a recent meeting of important doctors at St. Matthews Hospital, one cardiologist bravely voiced his concern that bypass surgery was performed too freely on too many patients in the hospital. The doctor was promptly and quietly asked to remove himself from the meeting. Several days later, he received a letter announcing his dismissal from the committee.

The silent conspiracy conducted by hospitals and cardiologists serves their own purposes better than the good of the public. Under the guise of good works, hospitals continue to promote strategies which are, for the most part, outdated, inefficient, inaccurate, and expensive. But that’s the rub. Expensive to you and your insurance company means more money for the recipient: your hospital and cardiologist, and the powers that support them. All this occurs while the real solutions that are of benefit to the public continue to be overlooked, hidden in the shadows.

Top Doctor

Dr. Robert Connors is the hospital’s most prized cardiologist.

Practically a fixture in the cath lab, he generates more revenues for the hospital than any of his colleagues. Last year alone, he performed over 1500 procedures, bringing in $18 million dollars to the cath lab, $27 million to the hospital. Dr. Connors is very good at what he does: 55-years old, he has been involved in high-tech heart care since the “early days,” 25 years ago, when hospital procedures really took off.

During his career, he has personally performed over 25,000 heart procedures and has built a reputation as a skilled operator of complex coronary procedures. Because of his skills, he enjoys a vigorous flow of referrals for procedures from dozens of primary care physicians. His skill has also earned him referrals from cardiologist colleagues who seek his abilities for difficult cases.

On any day, Dr. Connors typically schedules up to 12 procedures. His entire day is spent in the cath lab, usually from 7 am until 6 pm. He meets many patients for the first time on the catheterization laboratory table as staff shave their groin, preparing for the procedure. Much of the procedure itself is not even performed by Dr. Connors, but by one or another cardiologists-in-training, a “fellow,” or member of the fellowship the hospital proudly maintains as a clinical teaching institution. Nor will Dr. Connors talk to most patients at the close of the procedure. He leaves that to either the fellow or a nurse. Dr. Connors views himself as a procedural specialist, not someone who has to take care of patients. He gave up seeing patients in his office over 10 years ago.

Dr. Connors’ procedural enthusiasm gained him the attention of drug and medical device manufacturers. Because Dr. Connors lectures widely and advises colleagues, his comments can dramatically alter perceptions of the value of a technology. He has, on many occasions, catapulted an unpopular device to most-asked-for among colleagues, bringing millions in revenues to the manufacturer. One particularly lucrative arrangement he made around 10 years ago involved a “closure” device, a $400 single-use plug used to close the access site made during heart catheterizations. By swaying his colleagues at St. Matthews Hospital, 50 orders per day (one per procedure) tallied $20,000 every day, $7.1 million dollars per year for the manufacturer. Although he’d used other devices on the market, the 5,000 shares of stock he was offered encouraged him to issue glowing comments to colleagues on the superiority of this specific brand of closure device. Now over 90% of all catheterizations at St. Matthews conclude with the device manufactured by the company in which Dr. Connors maintains partial ownership.

Negative comments, on the other hand, topple other products when Dr. Connors sees fit to pan them. For this reason, device and drug manufacturers run straight to Dr. Connors to gain his good graces as soon as possible after a product is released into the market. Because the competition is just as likely to do the same, it has often come down to a bidding war, the company providing the most lucrative arrangement most likely to win.

Thus, Dr. Connors proudly boasts of how many times he has flown to Hawaii, Europe, and other exotic locations at industry expense. He also boasts of how, for $100,000 paid to him for a “consulting fee,” he can overturn the choice of products lining hospital shelves. As the hospital’s annual budget for coronary devices will top $84,000,000 this year, device manufacturers regard the sum paid Connors as a profitable investment.

Despite his lofty status in the hospital, Dr. Connors has long expressed a love-hate relationship with St. Matthews. While he enjoys his work and has made a more than comfortable income, he has long felt that the hospital administration didn’t truly appreciate his contributions. Five years ago, he therefore demanded that he be made “Director of Research.” After all, he had hired a nurse to help him coordinate enrollment of patients into several device trials brought to him by medical device manufacturers. When he encountered an initial lukewarm response from hospital administrators, he threatened to take his “business” elsewhere to a competing hospital. St. Matthews’ administrators gave in. They provided him with the title he wanted, along with $100,000 annual “stipend.”

True story, though names have been changed to protect the guilty.

Is Dr. Connors just an “outlier” among colleagues who toe a more conservative line? Or does his brand of commercial enterprise in hospital heart care represent the ideal that they seek, brazenly and ambitiously seeking to expand the procedural solution to heart disease to the exclusion of patient care and real human interaction?

Disease Engineering

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

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?

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”

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.