Apo E4 and sterols: Lethal combination?

Phytosterols, or just "sterols" to its friends and neighbors, are a group of cholesterol-like compounds that are abundant in the plant world. Lately, however, sterols have proliferated in the processed food supply, thanks to the observation that sterols reduce LDL cholesterol when ingested by humans.

This must mean that sterols are good for you.

Uh oh. Wait a minute: There is a rare disease called sitosterolemia in which there is unimpeded intestinal absorption of all sterols ingested through diet. They must have really low LDL cholesterols! Nope. They develop coronary disease--heart attacks, angina, etc.--in their late teens and 20s. In other words, if sterols gain access to your bloodstream, they are bad. Very bad.

Conventional thinking is that only a modest quantity of dietary sterols gain access to the bloodstream. But there are two potentially fatal flaws in this overly simplistic line of thinking:

1) What happens when you load up your diet with "heart healthy" sterols, such as those in "heart healthy" margarines, mayonnaise, and yogurt, effectively increasing sterol intake 10-fold?

2) What happens in people with the genetic pattern, apo E4, that is carried by 25% of the general population that permits much greater intestinal absorption of sterols?

My prediction: Despite the fact that sterols reduce LDL, they may, in certain genetically-susceptible people, such as those with apo E4, increase risk for heart disease: heart unhealthy.

Here are two studies that suggest that greater sterol absorption in people without sitosterolemia are at higher risk for heart disease:

Alterations in cholesterol absorption/synthesis markers characterize Framingham offspring study participants with CHD

Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study

Glucomania

As I suggested in a previous Heart Scan Blog post, a glucose meter is your best tool to:

1) Lose weight
2) Cure diabetes
3) Reduce or eliminate small LDL particles
4) Achieve anti-aging or age-slowing effects


But it means getting hold of a glucose meter and applying it in a very different way.

Diabetics typically check fasting morning glucose and again several times during the day to assess medication effects. But you and I can measure blood glucose to assess the immediate effects of food choices--two very different approaches.

The concept is simple: Check a blood glucose just prior to a food or meal of interest, then one hour after finishing.

Let's take two hypothetical breakfasts. First, oatmeal, a so-called "low-glycemic index" food. Slow-cooked, stone ground oatmeal with skim milk, a handful of walnuts, just a few blueberries.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 175 mg/dl

I made those numbers up, but this is a fairly typical response for many adults. (This is why "low-glycemic index" is an absurd notion.) This kind of response causes 1) glycation, the adverse effects of glucose modification of proteins that leads to cataracts, kidney disease, cartilage damage and arthritis, atherosclerosis, skin wrinkles, etc., 2) high insulin response that cascades into fat deposition, especially visceral fat ("wheat belly"), and 3) glucotoxicity, i.e., direct damage to the pancreas that can, over years, lead to diabetes.

Next day, let's try a breakfast of 3-egg omelet made with green peppers, sundried tomatoes, and olive oil.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 93 mg/dl

This is a meal of virtually zero-glycemic index. This kind of response triggers none of the effects experienced following the oatmeal. Repeated over time and you fail to trigger glycation, you stop provoking insulin, and visceral fat mobilizes rather than accumulates: you lose weight, particularly around the middle.

We therefore aim to keep the one-hour blood glucose 100 mg/dl or less. If you start with a high fasting blood glucose of, say, 118 mg/dl, then we aim to keep the one-hour after-eating blood glucose no higher than the pre-meal.

It works. Plain and simple.

This makes the primary care docs crazy: "How dare you check your blood sugar! You're not diabetic." In truth, blood glucose meters are relatively simple devices to use. The test strips and lancets will cost a few bucks. (The meters themselves are either low-cost or free, just like Gillette sometimes sends you a beautiful new razor for free but expects you to buy the blades). These are direct-to-consumer products. While a prescription written by your doctor for a glucose meter and supplies helps insurance cover the costs, you can easily get these devices without a prescription. Some stores, like Target, keep their devices out on the shelves with the shampoo and bath soap.

Warning: Anyone taking diabetes drugs will have to consult with their doctors about the safety of such an approach. Because this approach can actually cure diabetes in some people, if you are taking some diabetes drugs, especially glyburide, glipidize, and glimepiride, you can experience dangerously low blood sugars, just as any non-diabetic taking these drugs would.

Diarrhea, runny noses, and rage: Poll results

Here are the results of the week-long poll asking the question:

Have you experienced a wheat re-exposure syndrome?
Yes, undesirable gastrointestinal effects 223 (41%)

Yes, asthma or sinus problems 51 (9%)

Yes, joint pains and/or swelling 85 (15%)

Yes, emotional or other nervous system effects 59 (10%)
No, nothing, nada  107 (19%)

No. Wheat is sacred and you're all nuts  13 (2%)


There are several interesting observations to make from this informal poll. First, as I have observed, the most common wheat re-exposure syndrome is gastrointestinal, usually involving cramps, diarrhea, and lame explanations to your dinner partner.

Second most common: joint pains and/or swelling.

Third: asthma or sinus congestion.

The incidence of emotional or nervous system effects surprised me a bit. I didn't expect 10% of people to share this effect. This is an effect I also experience personally, along with the gastrointestinal consequences.

To be sure, this is a skewed poll, since many people likely come to this blog in the first place because of such issues. But I was nonetheless impressed with the relatively modest proportion of people who did not share such a re-exposure syndrome: only 19%.

Beyond the interesting numbers provided by readers, a good many also provided some fascinating and graphic comments. Here's a sample:




Sassy said:

Reflux -- starts a day later and goes for up to a week. And Bloat:2-5 inches on my waistline in a day, lasting up to three. Miserable. And why, having experienced this once, have I done it often enough to verify the connection with certainty? I am working on that one.



Anonymous said:
Wheat increased hunger with even with only a small amount. Crackers in soup was enough to set it off.

Also, when I was trying to get off wheat, I noticed that 2 eggs and 2 bacon and I could go 5 hours before hunger, or 2 eggs and 2 bacon and toast was good for three hours before hunger. That was the final step to giving up wheat. Now three years and 59 Kg [130 lbs!] loss later, there is no doubt in my mind that wheat is evil, and I do not regard it as suitable for human food. I speculate that it increases ghrelin or cortisol.

Anna said:
For me, in the two years since I began eating Gluten-Free (Low Carb for 6 years), the few times I've had re-exposure to wheat, I've experienced fast onset and intense abdominal pain (known exposure during the daytime) and heartburn, indigestion, intense nausea, and disrupted sleep (exposures during evening meal not discovered until the next day).

My husband wants to think he's fine with wheat (though I know that he has at least one gene that predisposes to celiac), but IMO, he isn't. He eats no wheat at home because that's the default, and he's OK with that. But if he goes out to dinner at a restaurant that serves "good" artisan bread, he will indulge in a few bites (he does restrict his carb intake, so it's still a limited amount). More often than not, he will sleep fitfully on those nights, snore more, and wake in the night with indigestion. He wants to bury his head in the sand and will only acknowledge the discomfort being due to eating too many carbs, not the wheat itself. I notice he sleeps fine if he eats a small amount of potato or rice. Go figure.

Our 12 yo son has been eating GF for two years also. About 6 months into GF, he unknowingly ate wheat a number of times (licorice candy laces at a friend's house), which resulted in outbreaks of canker sores in his mouth each time. He also exhibits mood and behavior changes when he eats wheat, which is what prompted me to test him for gluten intolerance in the first place.

Mark said:
If I go for 3-4 days without wheat, grains or sugar and then go out and binge on a pizza and ice cream or something like that I become explosive within 20 minutes to an hour. It's like a wheat and sugar rage.(I'm not saying this is an excuse for rage, I'm saying it has happened to me and I believe partly do to re-exposure) It seems the combination of the wheat plus sugar can be the worst.

I get red rashes around my neck sometimes right away and sometimes up to a day or later and sometimes get bad diarrhea. 
I think it can be almost dangerous to cut things like gluten and sugar suddenly out of the diet without being very serious about keeping them out. I have found it very hard to cut out wheat without binging on it later after 4 or 5 days. I don't believe that my symptoms are just psychological either.

I was also diagnosed with ADHD as a young kid and then rediagnosed with adult ADHD by 3 different doctors. I also have bouts of mania at times too. I am considering trying to go completely gluten/refined carbohydrate free to see if it helps with the symptoms and gives me some relief.

I have never been tested for celiac or gluten intolerance but I would like to be. I think it would help explain to my girlfriend, family and friends why I can't go out and eat pizza or have a beer or ice cream. Right now they all think I'm a hypochondriac. At times I have experienced an intense fatigue the next day like I can't wake up and also sharp pains in my body and headaches.

Anonymous said:
I ditched wheat a year ago after my wife was diagnosed celiac. I immediately experienced a number of health improvements (blood lipids, sleep, allergies, etc.).

Fast forward: We all suffered some inadvertent wheat exposure yesterday via some chocolate covered Brazil nuts (of all things). This accidental A-B-A experimental design resulted in the following:

1. My celiac wife experienced what she calls "the flip" within an hour of exposure (i.e., intense GI distress).
2. My five-year old son went to bed with some wicked reflux.
3. I woke up with some twinges in my lower back and an ache in my football-weary left shoulder. I was also complaining to my wife about fuzzy-headedness that refused to respond to caffeine or hydration. I could only describe it as "carb flu"...

And then I read your post!

Anne said:
Depression, agitation and brain fog if I get glutened. Some times this comes with abdominal pain and a rash on my back - I think it is dose dependent. Cross contamination with wheat is a big issue when eating out. Needless to say, I eat out infrequently and then try to stick with the restaurants that are the most aware of gluten issues.

Terrence said:
Several weeks ago, I started Robb Wolf's 30 day challenge.

The first two weeks were brutal - calling it a withdrawal flu was a massive understatement. So, I thought I would try some wheat and see what happened (could not be worse, I thought). Well, it was.

I still felt extremely crappy, but I was now MASSIVELY GASSY - AMAZINGLY GASSY, for about 48 hours - flatulence on wheels, in spades. I did not go out at all in those 48 hours - when the gas came on, it went out, LONG, and QUICKLY and LOUDLY.

I am easing back into wheat and grain free. I am gluten free today and tomorrow (Sunday and Monday). I expect to try a small amount of wheat on Thursday, then maybe a little more the following Thursday.

Donald said:
I have limited wheat consumption severely over the last 8 months. I have lost 120 pounds, no longer have bouts of illness, asthma, depression, or low energy. I also take vitamin D and other supplements that have helped (many are from your blog recommendations).

Last week I ate a small piece of cake and dessert pizza. Shortly thereafter I started sneezing, had a scratchy throat, and runny nose. I called off sick the next day for fear of being contagious. My symptoms subsided quickly and I am now attributing them to the processed flour eaten at my work luncheon. I think it was an allergic reaction since I recall having much more severe symptoms fairly regularly in my wheat eating days. Those were attributed to an "allergy" of unknown origin back then.

John said:
I suffered from Ankylosing Spondylitis, Iritis, Plantar Fasciits, etc for a number of years. I restricted carbs, especially wheat and I've been symptom free for the past two years now.

Lori said:
I found wheat to be one of the worst things for giving me gas bloating and acid reflux, and I'd had sinus and nasal congestion my whole life. When I ate that cookie, it just re-introduced old problems. I can occasionally eat a gluten-free, grainy goody at my party place without any side effects. I also have a little sprouted rice protein powder every day.

Another odd thing about wheat: it was hard for me to stop eating it once I started. I could go through a whole box of cookies in one sitting, even though I wasn't a binge eater. But I can have a couple of gluten-free cookies and stop.

Paul said:
Except for one slip up this recently past holiday season, I've been sugar-grain-starch free since July 2008. Mental fog was the most noticable re-exposure symptom I had.

My mom has had the worst acid-reflux for 40-plus years. It had become so bad that she was on three medications just to deal with the symptoms. After much training and coaxing, I finally got across to her 
how to totally get off wheat. Not at all to my surprise, after being wheat free for a few weeks, she lost weight and her acid reflux was GONE!

But she had been addicted to wheat for so long, she relapsed, and the reflux fire soon returned. Wheat must be akin to heroin with some people. Even though they know it's very bad for them, they can't help themselves.

Onschedule said:
Re-exposure often leads to diarrhea for me, or such a heavy feeling of tiredness that all I can do is lay down and pass out. A local pizzeria makes a darn good pie, but since I started practicing wheat-avoidance, I can't keep my eyes open after eating there. I can't say for sure that it's the wheat causing it, but definitely something in the crust. Diarrhea, on the other hand, is definitely triggered by the wheat for me.

My mom complained of gastric reflux for years, but never filled the prescriptions that her doctors would give her. I suggested wheat-avoidance- gastric reflux disappeared within 3 days and hasn't returned (has been 6 months now). I've already commented elsewhere on this blog about how much weight and bloating she has lost...

Steve said:
Interesting that I should sit down, turn on my computer and find your poll. Having gone several weeks, maybe months, avoiding gluten, I took my daughter and her boyfriend out to eat because my wife has been working late at the office lately. Although I was thinking I would just eat my steak and chicken, I succumbed to the temptation of eating about a dozen greasy, breaded shrimp that my daughter and her boyfriend ordered. It's 1:39am and I still do not feel sleepy. My left nostril is completely blocked, my stomach feels bloated, really, really full and I've been burping. In your poll I checked sinus problems but could have chose gastrointestinal or nervous problems just as well. 


A few weeks ago my daughter brought home a pizza and, once again, despite my knowing that I shouldn't, I ate a couple of pieces. I was sick for two days. The pain in what I think was my transverse colon was so bad I thought I might have to go to ther emergency room. Before I ate the pizza I had never gone grain-free that long before. I did this after reading Robb Wolf's book. 


I AM CONVINCED. No more wheat for me! Please, Lord, give me strength.

LV said:
What don't I experience! I typically avoid wheat (and gluten for that matter) as I'm pretty sure it makes me sick, but when I slip (or someone else slips me some) I end up with massive amounts of joint swelling and tenderness, diarhea, cramping, gas, bloating and brain fog. I'm absolutely miserable. Just that alone is enough to keep me off gluten. I have RA, so if I have repeated exposures I'll have a flare which SUCKS!

The perfect Frankengrain

Pretend I'm a mad food scientist. I'd like to create a food that:

1) Wreaks gastrointestinal havoc and cause intractable diarrhea, cramps, and anemia.
2) Kills some people who consume it after a long, painful course of illness.
3) Damages the brain and nervous system such that some people wet their pants, lose balance, and lose the ability to feel their feet and legs.
4) Brings out the mania of bipolar illness.
5) Amplifies auditory hallucinations in people with paranoid schizophrenia.
6) Makes people diabetic by increasing blood sugars.
7) Worsens arthritis, such as osteoarthritis and rheumatoid arthritis.
8) Triggers addictive eating behavior.
9) Punishes you with a withdrawal process if you try to remove it from your diet.

I will develop a strain that is exceptionally hardy and tolerates diverse conditions so that it can grow in just about any climate. It should also be an exceptionally high yield crop, so that I can sell it cheaply to the masses.

Now, if my evil scheme goes as planned, I will then persuade the USDA that not only is my food harmless, but it is good for health. If they really take the bait, they might even endorse it, create a diet program around it.

Dag nabit! Such a plan has already been implemented. Another evil food scientist already beat me to the punch. The food is called wheat.

Diabetes: A study in aging

Diabetics experience long-term health difficulties, including atherosclerosis/heart attacks, peripheral vascular disease, hypertension, cataracts, kidney disease, neuropathies, male erectile dysfunction, osteoarthritis, and colorectal cancer. They also die, on average, 10 years earlier than non-diabetics.

In effect, diabetics compress their lives into a shorter period of time. They experience all the "complications" of aging at a younger age. People without diabetes, of course, can develop atherosclerosis, cataracts, kidney disease, etc., but they tend to do so later in life compared to diabetics.

One index of the rate of aging (but not chronologic age itself) is hemoglobin A1c, or HbA1c, a "moving average" of glycated hemoglobin, i.e., glucose-modified hemoglobin. Blood glucose glycates hemoglobin linearly and irreversibly; measuring HbA1c thereby provides an index of the last 60 or so days average blood glucose.

To put HbA1c values into perspective:

Average HbA1c of hunter-gatherers: 4.5%
Average HbA1c for Americans: 5.6%
American Diabetes Association definition of diabetes: 6.5% or greater
American Diabetes Association definition of adequate control of diabetes: 7.0% or less

Why do diabetics age faster? There are likely several reasons. One important reason is glycation, as indexed by HbA1c. Glycated proteins in the lens of the eye causes cataracts. Glycated proteins in cartilage leads to arthritis. Glycated LDL particles (apo B) leads to atherosclerosis. Glycated nerve cells causes neuropathy. And so on.

If glycation underlies many of the phenomena of aging, then we might surmise that:

1) The less you glycate, the slower you age.
2) The more you glycate, the faster you age.

Therefore, the higher the HbA1c, the faster you are aging.

What foods increase HbA1c? Carbohydrates. That bowl of slow-cooked, stone ground oatmeal? A one-hour after-eating blood sugar of 170 mg/dl is common. Your doctor says that's okay because it's below 200 mg/dl and you don't "need" medication yet.

Fish oil: The natural triglyceride form is better

If you have a choice, the triglyceride form of fish oil is preferable. The triglyceride form, i.e., 3 omega-3 fatty acids on a glycerol "backbone," is the form found in the body of fish that protects them from cold temperatures (i.e., they remain liquid at low ambient temperatures).

Most fish oils on the market are the ethyl ester form. This means that the omega-3 fatty acids have been removed from the glycerol backbone; the fatty acids are then reacted with ethanol to form the ethyl ester.

If the form is not specified on your fish oil bottle, it is likely ethyl ester, since the triglyceride form is more costly to process and most manufacturers therefore boast about it. Also, prescription Lovaza--nearly 20 times more costly than the most expensive fish oil triglyceride liquid on a milligram for milligram basis--is the ethyl ester form. That's not even factoring in reduced absorption of ethyl esters compared to triglyceride forms. Remember: FDA approval is not necessarily a stamp of superiority. It just means somebody had the money and ambition to pursue FDA approval. Period.

Taking any kind of fish oil, provided it is not overly oxidized (and thereby yields a smelly fish odor), is better than taking none at all. All fish oil will reduce triglycerides, accelerate clearance of postprandial (after-eating) lipoprotein byproducts of a meal (via activation of lipoprotein lipase), enhance endothelial responsiveness, reduce small LDL particles, and provide a physical stabilizing effect on atherosclerotic plaque.

But if you desire enhanced absorption and potentially lower dose to achieve equivalent RBC omega-3 levels, then triglyceride forms are better.

Here are cut-and-pasted abstracts of two of the studies comparing forms of fish oil.

Bioavailability of marine n-3 fatty acid formulations.

Dyerberg J, Madsen P, Moller JM et al. 
Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark.

Abstract

The use of marine n-3 polyunsaturated fatty acids (n-3 PUFA) as supplements has prompted the development of concentrated formulations to overcome compliance problems. The present study compares three concentrated preparations - ethyl esters, free fatty acids and re-esterified triglycerides - with placebo oil in a double-blinded design, and with fish body oil and cod liver oil in single-blinded arms. Seventy-two volunteers were given approximately 3.3g of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 2 weeks. Increases in absolute amounts of EPA and DHA in fasting serum triglycerides, cholesterol esters and phospholipids were examined. Bioavailability of EPA+DHA from re-esterified triglycerides was superior (124%) compared with natural fish oil, whereas the bioavailability from ethyl esters was inferior (73%). Free fatty acid bioavailability (91%) did not differ significantly from natural triglycerides. The stereochemistry of fatty acid in acylglycerols did not influence the bioavailability of EPA and DHA.
(Full text of the Dyerberg et al study made available at the Nordic Naturals website here.)



Eur J Clin Nutr 2010 Nov 10. 

Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters.

Neubronner J, Schuchardt JP, Kressel G et al. 
Institute of Food Science and Human Nutrition, Leibniz Universität Hannover, Am Kleinen Felde 30, Hannover, Germany.

Abstract

There is a debate currently about whether different chemical forms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are absorbed in an identical way. The objective of this study was to investigate the response of the omega-3 index, the percentage of EPA+DHA in red blood cell membranes, to supplementation with two different omega-3 fatty acid (n-3 FA) formulations in humans. The study was conducted as a double-blinded placebo-controlled trial. A total of 150 volunteers was randomly assigned to one of the three groups: (1) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as reesterified triacylglycerides (rTAG group); (2) corn oil (placebo group) or (3) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as ethyl ester (EE group). Volunteers consumed four gelatine-coated soft capsules daily over a period of six months. The omega-3 index was determined at baseline (t(0)) after three months (t(3)) and at the end of the intervention period (t(6)). The omega-3 index increased significantly in both groups treated with n-3 FAs from baseline to t(3) and t(6) (P < 0.001). The omega-3 index increased to a greater extent in the rTAG group than in the EE group (t(3): 186 versus 161% (P < 0.001); t(6): 197 versus 171% (P < 0.01)). Conclusion: A six-month supplementation of identical doses of EPA+DHA led to a faster and higher increase in the omega-3 index when consumed as triacylglycerides than when consumed as ethyl esters.

Diarrhea, asthma, arthritis--What is your wheat re-exposure syndrome?

Have you experienced a wheat re-exposure syndrome?

As I recently discussed, gastrointestinal distress--cramps, gas, diarrhea--is the most common "syndrome" that results from re-exposure to wheat after a period of elimination.

Others experience asthma, sinus congestion and infections, mental "fogginess" and difficulty concentrating, or joint pains and/or overt swelling.

Still others say there is no such thing.

Let's take a poll and find out what readers say.

Marathoners, triathletes, and heart disease

Curious thing: People with lipoprotein(a) gravitate towards elite levels of exercise.

I tell my lipoprotein(a) patients that, if they want to see a lot of other people with lipoprotein(a), go to a marathon or triathlon.

This effect applies more to males than to females, just as the fascination with numbers seems to be confined to men, too. That's why I've posted in past about the "prototypical" lipoprotein(a) male.

I believe this is a big part, perhaps the only, reason why there seems to be a modest increased risk for cardiovascular events despite high exercise levels in marathoners. It has nothing to do with the exercise itself; it has to do with the kind of people who choose to exercise at this level.

The best fish oil

The best fish oils available are the liquid forms. Contrary to many people's expectations, the best liquid fish oils have no fishy odor or taste.

I use a lot of liquid fish oils because of the higher doses we use in the Track Your Plaque program, as well as our strategy of high-dose fish oil to reduce lipoprotein(a). Women, in particular, don't like taking the oodles of capsules required to achieve the higher doses we need. So the ladies really like the liquid forms.

The best liquid fish oils are non-fishy, highly-concentrated, and come in the better absorbed triglyceride form. Many capsules, including prescription Lovaza, are the less well-absorbed ethyl ester form. Several studies, such as this one, have now demonstrated that the naturally-occurring triglyceride form yields higher blood (RBC) levels of omega-3 fatty acids, likely due to more efficient digestion via pancreatic lipase.

While there are many good forms of fish oil and only a few bad, these are the best of the best:

Pharmax
The Pharmax Finest Pure Fish Oil with Essential Oil of Orange contains 1800 mg EPA + DHA per teaspoon. This is the preparation I've been taking.

Nordic Naturals
The Nordic Naturals lemon-flavored ProOmega Liquid contains 2752 mg EPA + DHA per teaspoon, the most concentrated of any fish oil I've seen.

(This list is not exclusive. These are just two brands I've used extensively with good results.)

These highly-concentrated, triglyceride forms are more expensive, due to their concentrated nature. 1 teaspoon Pharmax fish oil, for example, provides an equivalent quantity of omega-3 fatty acids as 6 standard fish oil capsules on a milligram for milligram basis, but more like 8 to 9 capsules when absorption efficiency is factored in. The triglyceride form is also more laborious to manufacture. On our Track Your Plaque Marketplace, our Pharmax 500 ml runs $58.95 list. (500 ml provides 100 teaspoons or 600-capsule equivalent.)

Note that, minus the protection of the capsule, liquid fish oils will oxidize if not refrigerated. So be sure to keep your liquid fish oil in the fridge.
All posts by william-davis

Weight loss and blood pressure

Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP).

The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise.

Blood pressure also shows a curious pattern that is largely dependent on age.

Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most.

How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop.

Why the age-dependent difference?

It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop.

But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals.

"I lost 30 lbs and my triglycerides went . . . up?"

Brad needed to lose weight.

At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly.

He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise).

Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats.

Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years.

His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"

Yes, I had said that. But I was oversimplifying.

The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides.

So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's.

Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau.

In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL.

I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it.

I call these changes "transitional" changes in lipids.

Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad.

Divorce court for the doctor-patient relationship?

The doctor-patient relationship has gone sour.

This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:

Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.

Exploitation of trust, my observation that the enormous gap in heart disease prevention between the woefully ignorant (by necessity) level of sophistication of the primary care physician and the procedure-obsessed cardiologist leads to an exploitation of humans-for-heart-procedures because of the failure to institute genuine preventive efforts.

Bait and switch , a description of how a minor test or symptom can reap a bonanza of medical testing; a $20 "screening" test yields $10's of thousands in hospital procedures. If it were entirely due to the imprecision of medical testing and detection of disease, that might be forgivable. But it often is not: It has become utterly distorted by the profit model.



Lest you think that I am a kook ranting off in some backwoods corner (Milwaukee), here are the comments of New York Times' Health Editor Tara Parker-Pope in a series called Doctor and Patient, Now at Odds:

Lately I've been hearing a lot from patients who are frustrated, angry, and distrustful of doctors. Their feelings speak to a growing disconnect between doctors and patients and worries that drug companies, insurance rules, and hospital cost-cutting are influencing the care and advice that doctors provide.

Research shows that even among patients who like their personal physicians, there is a simmering distrust of the medical system and the doctors who work inside it.


(There's also a series of candid video interviews with people who echo these sentiments.)

There are a number of reasons for this increasing "disconnect," some of them articulated by Ms. Parker-Pope, others detailed in my blog posts.

The solutions, however, will not be found by advancing technology: the newest robotic surgery, a better defibrillator, a new statin drug, the next best chemotherapeutic agent. It will not be found by adding a new wing to the hospital. It will not be found by the reorganization of healthcare delivery achieved by converting primary care and specialty practice into an arm of hospital care. It will not be improved by employing "hospitalists." It will not emerge from legislation controlling insurance company practices. It certainly will not come from increasing marketing dollars spent by drug companies (who make $4 for every $1 spent on direct-to-consumer marketing).

The solutions will come from shifting the idea of care from a paternalistic, "I'm the doctor and I'll tell you what to do" approach, to the doctor-as-advocate-and-supporter of the patient. The physician should act as someone with a particular sort of expertise that can advise a patient.

But a caveat: The patient MUST be informed.

Proper information will not originate with the doctor. It will originate with internet-based information portals and tools that help you understand the issues, often with far greater depth than your doctor could ever provide. The physician needs to accept this role, one of advocate, adviser, but not of being in charge, not of viewing the patient as profit-center, not as an opponent in a power struggle.

Sadly, the last few years in online information portals has been dominated by the drug company-dominated websites like WebMD, nothing more than a deliverer of the conventional wisdom with nothing whatsoever aimed towards empowering patients in a self-directed healthcare model.

Some people call the emerging new empowered and information-armed patient Medicine 2.0. Unfortunately, Medicine 2.0 will first benefit the intellectual upper crust of Americans, the web-savvy and motivated to engage in health issues. But, give it 10 years, and we will witness the effects on an unprecedented broad scale. Part of the Information Age is acceleration of information dissemination. Imagine your children, facile with a computer mouse, posting comments on FaceBook, doing homework with Google and Wikipedia, now turning their attentions to health.

It will be a startling change.

In the meantime, be wary. Be empowered. Think increasingly about self-direction in your health.


In a comment to the Bait and switch post, Jennytoo offered an insightful response:

You are getting to the essence of the problem, and it's not just cardiology that is rife with what is, at bottom, malpractice.

There is little incentive for the profession as a whole to know anything about or promote prevention, and many incentives from hospitals, drug and insurance companies to stick with the status quo or to change it in their corporate favor. The formulaic, conventional statements purporting to be guidelines for prevention that are put out by various interest groups and in such publications as hospital-sponsored newsletters ("eat a 'balanced diet', avoid stress, etc.") are useless sops to the concept of prevention.

It is, and I fear is going to remain, up to motivated individuals, both physicians and patients, to reshape the system, and it's going to be a long frustrating struggle.

It's my personal conviction that if just 4 things were promoted to the public, and people actually practiced them, we could change the health profiles of the majority of people in this country for the better within two years or less. They are:

(1) education on and promotion of a true low-carbohydrate, whole foods, diet,
(2) measurement and supplementation of Vitamin D3,
(3) supplementation with DHA/EPA (found in Fish Oils), and
(4) measurement and supplementation of intracellular magnesium.

I am not a health professional, and others may want to add to this list, but I don't think any strong case can be made against any of the items. The wonderful and hopeful thing is that each of us can implement them ON OUR OWN, and thereby take charge of our own well-being. (The Life Extension Foundation is one organization which provides access to lab tests you can request on your own.)

If you have a physician who is willing and capable of being your partner, you are richly blessed, and that is the ideal we all should hope for. But in the more likely event that you do not have such a physician, and if your physician demonstrates little potential for becoming one, think about firing the one you have and finding another.

Sometimes we are forced by circumstances, particularly urgent ones, to deal with physicians who are not ideal, but the main impetus for change will come from us, the patients, and the expectations we communicate to our individual doctors. In the meantime, we can be self-reliant in our own prevention practices.


Wow. A woman after my own heart.

How much fish oil is enough?


This post just furthers this line of thinking out loud: How much fish oil is "enough"?

Observations over the last 30 years followed this path: If a little bit of omega-3 fatty acids from fish are beneficial in reducing cardiovascular events, and a moderate intake is even better, is even more better? When have we reached a plateau? When do adverse effects outweigh the benefits?

Some insight can be gained through studies that examined blood levels of omega-3s. Let's take a look at some data from 2002, a comparison of men dying from heart disease vs. controls in the Physicians' Health Study, Blood Levels of Long-Chain n–3 Fatty Acids and the Risk of Sudden Death.

This is a table that shows the blood levels of various fatty acids Group with sudden death vs Control Group:




Several observations jump out:

--The total omega-3 blood content differed significantly, 4.82 vs 5.24% ("Total long-chain n-3 polyunsaturated")
--Total omega-6 content did not differ
--Arachidonic acid (AA) content did not differ
--Linolenic acid content did not differ (i.e., plant sourced omega-3)

The fact that neither omega-6 nor arachidonic acid content differed counters the argument that Simopoulos has made that the omega-6 to omega-3 ratio (intake, not blood levels) is what counts. It also argues against the EPA to AA ratio (and similar manipulations) that some have argued is important. In this study, only the omega-3 level itself made a difference; no ratio was necessary to distinguish sudden death victims vs controls.

Further, quartiles of omega-3 blood levels showed graded reductions of risk:




An omega-3 blood level of 6.87% conferred greatest risk reduction. Depending on the model of statistical analysis, risk reductions of up to 81-90% were observed. Wow.

Taken at face value, this study would argue that:

--An omega-3 fatty acid blood level of 6.87% (or greater?) is ideal
--The omega-3 fatty acid blood level stands alone as a predictor without resorting to any further manipulation of numbers, such as relating EPA and/or DHA to AA levels.

Of course, this is just one study, though an important one. It is also not a study based on any intervention, just an observational effort. But it does add to our understanding.


We will develop these issues further in our upcoming Track Your Plaque Webinar on Wednesday, August 20th, 2008.

Omega-6 / omega-3 ratio

Most of us already know that the intake of omega-6 fatty acids in the American diet has gone overboard, much at the expense of the omega-3 fraction. This occurred as a result of the misguided advice of the 1970s and 1980s to eat polyunsaturated oils like corn, sunflower, and safflower, because of their presumed cholesterol-reducing properties compared to saturated fats. However, more recent examinations of this advice have suggested that the omega-6 fraction of oils present in polyunsaturated oils may amplify arachidonic acid and other inflammatory patterns despite the reduction in cholesterol (total and LDL).

Dr. Artemis Simopoulos of the Center for Genetics, Nutrition and Health in Washington, D.C. has written extensively on the role of omega-6 and omega-3 fatty acids in diet.

In a review entitled The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cadiovacular Disease and Other Chronic Disease , Dr. Simopoulos collects the following comparison of omega-6 to omega-3 ratios from various populations:


Paleolithic humans 0.79
Greece (prior to 1960) 1.00-2.00
Current Japan 4.00
Current India, rural 5-6.1
Current United Kindom and northern Europe 15.00
Current United States 16.74
Current India, urban 38-50

(The numbers refer to the ratio of omega-6 to omega-3 intake.)


If we believe the observations of Dr. Loren Cordain and others, while paleolithic man died of trauma and infectious diseases, they did not die of heart disease. Paleolithic human intake of omega-3 exceeded that of omega-6.

Likewise, the traditionally low cardiac event regions of the world like Japan and Greece have less omega-3 intake than Paleolithic man, but still many times more than the U.S. and U.K.

Worst of all with an enormous preponderance of omega-6 over omega-3 are urban Indians, who experience among the highest rates of heart disease in the world.

Just for perspective, let's assume you eat an 1800 calorie per day diet, of which 30% of calories come from fat. This would amount to 540 calories per day from fat. With 9 calories per gram of fat, this means that there are 60 grams, or 60,000 mg, of fat in your diet per day.

Paleolithic man has been found to have existed on a diet consisting of 21% of calories from fats. Again assuming an 1800 calorie per day diet, that comes to 42 grams of fat per day (42,000 mg).

If we were to try to recreate the Paleolithic fat composition of diet, we would ingest 21,000 mg of omega-3 fatty acids (EPA, DHA, linolenic acid) per day. Even recreating a Japanese experience with a 4:1 ratio, it would mean 8400 mg of omega-3 per day. (Curiously, this does not agree with all estimates of Japanese intake of omega-3s.)

No matter how you look at it, cultures with lower rates of cardiovascular disease take in greater--much greater--quantities of omega-3 fatty acids.

So don't complain about your six fish oil capsules (usually containing 6000 mg of total oil, 1800 mg omega-3s)!

Dr. Bernadine Healy on heart scans


A Heart Scan Blog reader brought the following tidbit to my attention.

Cardiologist and now writer for U.S. News and World Report, Dr. Bernadine Healy, wrote this editorial, a glowing endorsement of heart scans:

The approach is beautifully simple. Calcium accumulates in advanced plaques, so calcium visible in the heart's arteries indicates atherosclerosis. An exploding number of studies in the past few years have unequivocally shown that the calcium score predicts both heart attack and sudden death. As a generalization, patients with scores between 100 and 400 face three to four times the risk of a heart attack or death compared with others at the same age with a zero score. Over 400, that elevated risk more than doubles.

Most doctors rely instead on the Framingham calculator, which estimates a symptom-free person's risk of a heart attack in the next 10 years based on smoking history, blood pressure, cholesterol levels, sex, and age. It's available free online from the National Institutes of Health. Most people taking the test will have minimal or no coronary disease, though risk estimates over 9 percent should inspire vigorous preventive efforts. For some, however, coronary heart disease is sneaky, and Framingham will underestimate what lies ahead. Roughly half of those who suffer a major heart attack or sudden coronary death are symptom free. Calcium scores are additive to Framingham; they pick up the individual surprises by using X-ray vision to look inside the heart. No wonder insurance companies are scrambling to use coronary calcium scores—life insurers, that is.



Dr. Bernadine Healy is no small-time player. In addition to her academic credentials, she is former chief of the National Institutes of Health (the first woman to hold the influential post), former head of the American Red Cross, and former deputy director of the White House Office of Science and Technology Policy under the Reagan administration. An endorsement of CT heart scans, though written under the guise of a probing editorial, will do an enormous amount of good to overcome the hurdles in gaining wider acceptance of heart scans.

Those of us applying heart scans in everyday practice have long appreciated their enormous power to detect and track coronary plaque. Framingham scoring can't even touch the certainty and quantification provided by heart scans in day-to-day life. Hundreds of studies have validated their use, but they still suffer from lying in the shadows of the procedural bullies aiming to boost the number of heart catheterizations, angioplasties, stents, bypass surgeries.

Dr. Healy, a voice with great weight, not just a political figure but also a cardiologist and scientist, has done a great service to broadcast the message of heart scanning.

Mercury and fish oil

As time passes, the dose of fish oil advocated in the Track Your Plaque program is going upward.

While epidemiologic studies, like the Chicago Western Electric Study and the Nurses' Health Study suggest that decreases in mortality from heart disease begin by just eating fish a couple times per month, there are newer data that suggest greater quantities confer greater benefits.

In the last Heart Scan Blog post, I discussed the recently-released ERA JUMP Study that demonstrated a relationship between higher omega-3 fatty acid blood content and reduced quantities of carotid and coronary plaque. The JELIS Study demonstrated a 19% reduction in cardiovascular events when fish-consuming Japanese added 1800 mg of EPA (only).

However, the suggestion that increased quantities of fish oil potentially yield greater protection from heart attack and facilitate coronary plaque regression is also stirring up worries about mercury exposure. So I dug up a Heart Scan Blog post from a year ago that discussed this issue and reprint it here.


I often get questions about the mercury content in fish oil. I've even had patients come to the office saying their primary care doctor told them to stop fish oil to avoid mercury poisoning.

Manufacturers of fish oil also make claims that this product or that ("super-concentrated", "pharmaceutical grade", "purified", etc.) is purer or less contaminated than competitors' products. The manufacturers of the "drug" Omacor [now Lovaza], or prescription fish oil, have added to the confusion by suggesting that their product is the most pure of all, since it is the most concentrated of any fish oil preparation (900 mg EPA+DHA per capsule). They claim that "OMACOR is naturally derived through a unique, patented process that creates a highly concentrated, highly purified prescription medicine. By prescribing OMACOR® (omega-3-acid ethyl esters), a prescription omega-3, your doctor is giving you a concentrated and reliable omega-3. Each OMACOR capsule contains 90% omega-3 acids (84% EPA/DHA*). Nonprescription omega-3 dietary supplements typically contain only 13%-63% EPA/DHA."

How much truth is there in these concerns?

Let's go to the data published by the USDA, FDA, and several independent studies. Let's add to that the independent (and therefore presumably unbiased) analyses provided by Consumer Reports and Consumer Labs (www.consumerlab.com). How much mercury has been found in fish oil supplements?

None.

This is different from the mercury content of whole fish that you eat. Predatory fish that are at the top of the food chain and consume other fish and thereby concentrate organic methyl mercury, the toxic form of mercury. Thus, shark, swordfish, and King mackerel are higher in mercury than sardines, herring, and salmon.

The mercury content of fish oil capsules have little to do with the method of processing and much more with the animal source of oil. Fish oil is generally obtained from sardines, salmon, and cod, all low in mercury. Fish oil capsules are not prepared from swordfish or shark.

Thus, concerns about mercury from fish oil--regardless of brand--are generally unfounded, according to the best information we have. Eating whole fish--now that's another story for another time. But you and I can take our fish oil to reduce triglycerides, VLDL, IDL, small LDL, and heart attack risk without worrying about mercury.



I am not advocating ad libitum eating of fish. Sadly, this may be related to excessive accumulation of contaminants. I am suggesting that greater quantities of omega-3 fatty acids from relatively contaminant- and mercury-free fish oil capsules.

More on this in an upcoming webinar on the Track Your Plaque website: Fish Oil and the Track Your Plaque Program - Is More Better?

ERA JUMP: Omega-3 fatty acids and plaque


The results of the uniquely-constructed ERA JUMP Study were just released, a fascinating study of the relationship of omega-3 fatty acids to coronary and carotid plaque.

The study adds insight into why the Japanese experience only one third of the heart attacks of Americans, and why Japan occupies the bottom of the list for least heart attacks among all developed countries.

The Electron-Beam Tomography, Risk Factor Assessment Among Japanese and U.S. Men in the Post-World War II Birth Cohort Study (ERA JUMP), a collaborative U.S.-Japanese effort, compared three groups of men:

-- 281 Japanese men living in Japan
-- 306 non-Japanese men living in the U.S. (Pittsburgh, Pennsylvania)
-- 303 Japanese Americans (having both parents Japanese without “ethnic admixture”) living in Hawaii.

The last group represents a group that is genetically similar to the group in Japan, but exposed to an American diet and lifestyle.

Three main measures were compared:

-- Blood levels of omega-3 fatty acids, EPA and DHA)
-- Carotid intimal-medial thickness (CIMT, the thickness of the carotid artery lining that can serve as an index of body-wide atherosclerosis)
-- Coronary calcium (heart scan) scores.

Interestingly, at the start of the study, the Japanese men possessed an overall cardiovascular risk profile worse than the Americans: Though more slender (BMI 23.6), Japanese men were more likely to be smokers, alcohol drinkers, had more high blood pressure, and were less likely to take cholesterol medications. The Americans, conversely, although heavier (BMI 27.9), were less likely to be smokers and drinkers, and had a four-fold greater use of cholesterol medications.

The Japanese Americans were the most likely to be hypertensive, diabetic, with a similar proportion of overweight as the non-Japanese Americans.

Despite the overall greater heart disease risk for profile for Japanese men, compared to non-Japanese Americans they had 10% less CIMT. In addition, only 9.3% of Japanese men had abnormal coronary calcium scores vs. 26.1% of non-Japanese Americans. Japanese-Americans were the worst, however, with nearly 10% more CIMT than non-Japanese Americans and 31.4% with abnormal calcium scores.

The most intriguing finding of all was the fact that, of all the various groups and degrees of atherosclerosis, whether gauged via CIMT or coronary calcium scores, the blood level of omega-3 fatty acids was inversely related, i.e., the greater the omega-3 blood level, the less plaque by either measure was detected.

Japanese men had the highest omega-3 blood levels: twice that of the non-Japanese Americans. The Japanese-Americans had levels only slightly greater than non-Japanese Americans.

While other studies, like the GISSI Prevenzione study, have persuasively demonstrated that omega-3 fatty acids substantially reduce heart attack, a weak link in the omega-3 argument has been a study that links greater omega-3 intake with less atherosclerosis. The unique construction of the ERA JUMP Study, employing two groups with sharply different omega-3 intakes, very powerfully argues for the plaque-inhibiting effects of this fraction of fats.

How much omega-3 fatty acids do Japanese people eat? Estimates vary, depending on part of the country, coastal vs. inland, age, etc., but Japanese tend to ingest anywhere from 5 to 15-times more omega-3 fatty acids than Americans. The actual intake of omega-3 fatty acids (EPA +DHA) in Japanese ranges from 850 to 3100 mg per day.

Mediterranean diet and blood sugar


Data such as that from the Lyon Heart Study have demonstrated that a so-called Mediterranean diet substantially reduces risk for heart attack.

But there are aspects of the Mediterranean diet and lifestyle that are not entirely sorted out.

For instance, what specific component(s) of the diet provide the benefit? Is it olive oil and linolenic acid? Is it red wine? Is it the reduced exposure to processed snack foods that Americans are indundated with? Is it their more slender builds and greater tendency to walk? How about exposure to the Mediterranean sun? What about the inclusion of breads, since in the Track Your Plaque program I advocate elimination of wheat products for many abnormalities?

Anyway, here's a wonderfully thoughtful set of observations from Anna about her experiences traveling Italy, trying to understand the details of the Mediterranean diet while also trying to keep blood sugar under control.


I just returned from a two week stay in Italy, doing a bit of my own "Mediterranean Diet" experiments. When practical, we sought out food sources and places to eat that were typical for the local area, and tried as much as possible/practical to stay away from establishments that mostly catered to tourist tastes. I was really curious to see how the mythical "Mediterranean Diet" we Americans are urged to follow compared to the foods really consumed in Italy.

The first week, we stayed in a rural Tuscan farmhouse apartment (agriturismo), so many, if not most of our meals were prepared by me with ingredients I bought at the local grocery store (Coop) or the outdoor market in Siena. In addition, I purchased really fantastic free-range eggs from the farm where we were staying. (Between some language issues and seasonality, eggs and wine were what we could buy from them - though I was tantalized by the not-quite-ripe figs heavy on many trees). Mostly, our meals consisted of simple and easily prepared fresh fruits and vegetables, rustic cured meats (salami, proscuitto, pancetta, etc.) hand-sliced at the deli down the road, fresh sausages, various Italian cheeses, plus plenty of espresso. It was a bit disappointing to find underripe fruit & tomatoes as well as old green beans in the grocery stores, not to mention too many low fat and highly processed foods, but all over Europe the food supply is becoming more industrialized, more centralized, and homogenous, so I'm not too surprised that it happens even in Italy. But even with the smaller grocery store size, the amount of in-season produce was abundant, yet one still was better off shipping from the perimeter of the store, venturing into the aisles only for spices, olive oil, vinegar, coffee, etc. Without the knowledge of where to go and the language to really talk in depth about food with people, I wasn't able to find truly direct and local sources for as many foods as I would have liked, but still, we ate well enough!

The first week I maintained blood sugar levels very similar to those I get at home, because except for the Italian specialties, we ate much like we always do. A few rare exceptions to my normal BG tests were after indulging in locally made gelato or a evening limoncello cordial, but even then, the BG rise was relatively modest and to me, acceptable under the circumstance. Even with the gelato indulgences, it felt like I might have even lost a few pounds by the end of the first week and my FBG didn't rise much over 100.

The second week we stayed in two cities (Florence & Rome), and I didn't prepare any of my own food because I didn't have a kitchen/fridge. I found it impossible to get eggs anywhere for breakfast, and the tickets our hotels provided for a "continental" breakfast at a nearby café/bar was always for a coffee or hot chocolate drink and some sort of bread or roll (croissant, brioche, danish, etc.). At first I just paid extra for a plate of salami and cheese if that was available - or went to a small grocery store for some plain yogurt, but then I decided to go off low-carb and conduct a short term experiment, though I didn't consume nearly as many carbs as a typical Italian or tourist would.

So I breakfasted with a brioche roll or plain croissant for breakfast with my cappuccino, but unfortunately no additional butter was available. I didn't feel "full" enough with such a breakfast and I was usually starving an hour or two later. Additionally, when I ate the "continental" breakfast, I noticed immediate water retention - my ankles, lower legs, and knees looked like someone else's at the end of a day walking and sightseeing, swollen heavy. Exercising my feet and lower legs while waiting in lines or sitting didn't seem to help.

Food is much more expensive in Europe than in the US, and the declining US$ made everything especially expensive (not to mention the higher cost of dining out rather than cooking at home), so we tried to manage food costs by eating simple lunches at local take-away places, avoiding the corporate fast food chains. I was getting tired of salami/proscuitto & cheese plates, but the typical "quick" option was usually a panini (sandwich). At first I tried to find alternatives to paninis, but the available salads were designed for side dishes, not main meals and rarely had any protein, and the fillings of the expensive sandwiches were too skimpy to just eat without the bread. So I started to eat panini, although I sometimes removed as much as half of the bread (though it was nearly always very excellent quality pan toasted flatbreads or crusty baguette rolls, not sliced America bread). So of course, my post-prandial BGs rose, as did my FBG. I also found my hunger tended to come back much too soon and I think overall I ate more than usual in terms of volume.

Then we deviated from the "Italian" lunch foods and found a better midday meal option (quick, cheaper, and easier to customize for LC) - stopping at one of the numerous kebab shops and ordering a kebab plate with salad, hold the bread (not Italian, but still Mediterranean, I guess). I felt much better fueled on kebab plates (more filling and enough protein) than paninis, though I must say I still appreciated the taste of caprese paninis (slices of fresh mozzerella and tomato, basil leaves, mustard dressing on crusty, pan-toasted flat bread). If I followed my appetite, I could have eaten two caprese paninis.

We had some great evening dinners, at places also frequented by locals. This often was a fixed price dinner of several courses ("we feed you what we want you to eat"). Multi-course meals included house wine, and invariably consisted of antipasta (usually LC, such as a cold meat and cheese plate), pasta course (much smaller servings than typical US pasta dishes), main course plus some side vegetables, and dessert/coffee. These were often the best meals we experienced, full of local flavor and tradition (sometimes with a grandmotherly type doing the cooking), and definitely of very good quality, though we noticed the saltiness overall tended to be on the high side. I ate from every course, including some of the excellent bread (dipped in plenty of olive oil) and usually about half of the pasta served (2 oz dry?), plus about half of the dessert. After these meals I always ran BGs higher than usual, varying from moderately high (120-160 - at home I would consider this very high for me) to very high (over 180). By late in the week, my FBG was into the 115 range every morning (usually I can keep it 90-100 on LC food). Nearly everything that week was delicious, well-prepared food, but the high carb items definitely were not good for my BG control in the long run.

And most days I was doing plenty of walking, sprinting for the Metro subway trains, stair climbing (4th and 5/6th floor hotel rooms!), etc. but since I didn't have my usual housework to do, it probably wasn't too different from my usual exertion level.

So it was very interesting to experience the "Mediterranean Diet" first hand. Meats and cheeses were plentiful, fruits and vegetables played a much more minor role (main courses didn't come with vegetables other than what was in the sauce, but had to be ordered as additional items), but the overall carbs were decidedly too many. As I expected, it wasn't nearly as pasta-heavy as is portrayed in the US media/health press, but it is still full of too much grain and sugar, IMO. Low fat has become the norm in many dairy products, sadly, and if the grocery stores are any indication, modern families are gravitating towards highly processed, industrial foods. Sugar seems to be in everything (I quickly learned to order my caffe freddo con panno or latte sensa zuccero - iced coffee with cream or milk without sugar) after realizing that adding lots of sugar was the norm).

And, after several days of breakfasting at the café near our Rome hotel (where carbs were the only option in the morning), I learned that our very buff, muscular, very flat-stomached, café owner doesn't eat pasta (said as he proudly patted his 6 pack abs). I probably could have stuck closer to the carb intake I know works better for my BG control, but I figured if I was going to go off my LC way of eating and experiment, this was the time and place.

And yes, there were far fewer really obese people than in the US and lots of very slender people, but I could still see there were *plenty* of overweight, probably pre-diabetic and diabetic Italians (very visible problems with lower extremities, ranging from what looked like diabetic skin issues, walking problems, acanthosis nigricans, etc.). Older people do seem to be generally more fit than in the US (fit from everyday life, not exercise regimes), but there were plenty of "wheat bellies" on men old and young, even more young women with "muffin tops", and simply too many overweight children (very worrisome trend). So it may well be more the relaxed Italian way of living life (or a combination of other factors such as less air conditioning, strong family bonds, lots of sun, etc?) that keeps Italian CVD rates lower than the American rates, more than the mythical "Mediterranean diet".

Who is your doctor?


Primary care physicians are the initial entry point for healthcare for the majority of Americans.

Develop pneumonia; go to your family or internal medicine physician (internist) to be prescribed an antibiotic. Need your blood pressure or cholesterol checked? Develop a sore knee or swelling in your leg? Once again, go to your primary care physician.

Image courtesy Dedde'


Primary care physicians are a patient’s guide to a bewildering array of technology and specialists. If you require a specific diagnostic test or consultation with a specialist, your primary care physician will help you navigate through the maze, choosing the path that is best for you. He or she will order a chest x-ray for a cough and fever, provide vaccines to prevent flu or pneumococcal pneumonia, perform an annual physical. If you require hospitalization, your primary care physician will admit you. He or she will order diagnostic tests like MRI’s, ultrasounds, x-rays, and blood testing, usually performed in the hospital or a hospital-owned facility. If you require the services of a gastroenterologist, orthopedist, general surgeon, or neurologist, your primary care physician will refer you to the appropriate specialist.

That’s how it’s supposed to work, at least in principle. In fact, during the first eight decades of the 20th century, it did work that work way for the most part. Your primary care physician acted not just as a provider of healthcare, but as your advocate, someone who knew you and worked to protect your welfare. Your family doctor often knew your parents, maybe even delivered you at birth, and cared for your children. His children often went to the same schools as your children. He and his family lived in the same town and sometimes went to the same church.

That hardly happens any more. It’s more likely you got the name of your primary care physician from a doctor referral service provided by a hospital. Or you picked a name off a list provided by your health insurer. It’s also common to see one doctor, only to see another a year later. Two, three, or more different primary care physicians over a five-year period are common. Doctors come and go, since physician turnover in clinics and practices has been on the increase for years. Insurance companies frequently force policyholders to change doctors, requiring you to choose from a list.

The end result of this shuffling of primary care is increasing impersonality of the relationship. You probably don’t know your primary care physician outside of the 10-minute interaction you had six months ago. She probably never met your mother and will likely not care for your children. Two years from now, she will likely not be your doctor any more, replaced by someone else who obtains the details of your health from a chart. Your chart is more likely to be electronic, with the details of your health history listed in a checklist. There’s little room to detail the idiosyncrasies and quirks of your unique personality or health profile. Throw into this impersonal equation the fact that many doctors have become scared of patients because of potential for lawsuits, often over the most trivial of issues, or because of an error of oversight or misdiagnosis.

This flawed and impersonal system, though emotionally unsatisfying, can still work if each doctor who assumes a patient’s care maintains the ethic of putting health and welfare above all.

But what if your primary care physician is not just an advocate for your welfare, but is a representative of the hospital? What if there are hidden, unspoken financial incentives paid to your doctor to direct you to the hospital for diagnostic testing, hospitalization, and referral to specialists? If a headache becomes a $4800 MRI, or chest pain becomes a $4200 nuclear stress test, then a $14,000 heart catheterization, your primary care physician becomes the purveyor of far greater financial opportunity for the hospital. The entire interaction, founded on the proposition that your doctor actually cares about you, collapses in a heap of financially motivated testing and procedures. It appears to work, and you and your family can still obtain access to healthcare. The problem is that you’re likely to get too much of it.

This message has not been lost on the shrewd administrators at hospitals. Take a look at the ranks of primary care physicians who refer patients to some of your local hospitals. It is typical that a hospital system maintains several hundred primary care physicians on their payroll, all of whom are expected to refer patients to the hospital, cardiologists, and other proceduralists. Why so many?

Most primary care physicians today have signed contracts with a hospital. In other words, they are employees of the hospital. This practice is not unusual: the American Medical Association reported that 4 of 5 primary care physicians are now bound by such employment arrangements across the U.S. In effect, 80% of primary care physicians are legally bound by contract to direct patients to cardiologists who work at hospitals.

On top of contractual obligations, there are financial incentives for the volume of procedures that are generated as a result of referrals. The more procedures generated from an internist’s or family practitioner’s practice, the greater the end-of-year productivity bonus will be, not uncommonly totaling tens of thousands of dollars. Dr. Ted Phillips (not his real name, since he declined to allow me to use it) received a bonus check of $9,437 this year for his “productivity,” defined murkily as the return on specialist referrals. While the bonus may have helped him pay for his son’s college tuition, it clearly was a situation that made him acutely uncomfortable when asked.

Several primary care physicians are also quietly dismissed every year from the ranks of employed physicians for not maintaining a minimum flow of patients into the system.

Another hazardous point of entry: Many patients enter the hospital through the emergency room (ER). A patient in the emergency room is at his or her most vulnerable, seeking help for an urgent complaint and usually willing to accept whatever the ER physician advises. Hospitals know this. That’s why many systems insist that the ER physicians be employees of the hospital, with their practice habits subject to control. A patient goes to the ER with chest pain or breathlessness. The worst thing that can happen from a financial standpoint is for the patient to be evaluated and discharged. For this reason, a growing number of hospitals employ ER physicians, then proceed to legislate practice patterns. Consulting a cardiologist is strongly encouraged, since they generally provide access to the downstream revenue-producing procedures offered in the hospital. That way, what might have been a four hour, $2500 ER visit is converted into a $10,000 to $40,000 hospital stay, even when nothing was wrong in the first place. There are millions of people nationwide who have the hospital bills to prove it after being discharged with a diagnosis of indigestion.

Caveat emptor: Buyer beware.
All posts by william-davis

More on being wheat-free

Reducing or even eliminating the wheat in your diet can dramatically enhance the phenomenon of insulin resistance.

Insulin resistance is the evil process that lies behind low HDL, high triglycerides, small LDL particles, and VLDL and IDL. It’s also the process that makes us tired after meals, heightens inflammation that raises your risk of heart disease, stroke, diabetes, and caner. Insulin resistance is the culprit behind the bulge hanging over some 100,000,000 American belts.

Show me a person with a protruding abdomen and I’ll show you a bread lover, or some other form of wheat.

Why do I pick on wheat so much? Many of you among the more nutrition-minded would point out that wheat is just one group of food items among many other high-glycemic index foods, i.e., foods that yield a vigorous surge in blood sugar (glucose), followed by a sharp decline. Wheat enjoys the high-glycemic index company of corn, rice (white and brown), potatoes, among others.

I pick on wheat because, for most Americans, wheat is 90% of the high-glycemic index problem. (I’m assuming you’ve at least eliminated or dramatically reduced highly-processed sweets like candy, cookies, soft drinks, cakes, etc. That’s a no-brainer.) It’s not uncommon to have a wheat-based product with every meal, a wheat-based snack, 7 days a week. But few people have corn products (i.e., corn starch products) three times a day. Or rice three times a day.

Wheat has traded places with saturated fat sources as the chief scourge of diet. In 1985, we had dinners of spare ribs, cheeseburgers, French fries, and butter on our mashed potatoes. Hardly anybody eats that like anymore, at least amongst the web-savvy set.

Wheat has assumed the previous exalted role as chief scourge as a consequence of the low-fat consciousness of the 80s and 90s. It has since ballooned in importance in diet and, as a result, skyrocketed as a cause of obesity, insulin resistance, and coronary plaque growth.

What if you're already slender and have none of the above issues, especially small LDL particles? Then don't sweat the wheat issue.

Note: My comments on being wheat-free should not be confused with gluten sensitivity or celiac disease. These are allergies to wheat gluten that, if undiagnosed, wreak havoc on health to extremes. This phenomenon is separate and distinct from the far more prevalent issue I’m discussing.

Can you break the “Rule of 60”

In the Track Your Plaque program, we aim for conventional lipid values (LDL cholesterol, HDL cholesterol, and triglycerides) of 60—60—60, i.e., LDL 60 mg/dl, HDL 60 mg/dl or greater, triglycerides 60 mg/dl. Most participants do indeed reach these target values.

When I tell this to colleagues, they’re stunned. “You can’t possibly get those numbers in most people.” And I can sympathize with their plight. After all, they are stuck with relatively lame tools: statin drugs, the American Heart Association diet. I’d be surprised if they ever achieved 60—60—60.

But can you drop your heart scan score even if you don’t reach the 60—60—60 targets? Yes, you can. The Rule of 60 is only a guideline, a tool that helps more people achieve our goals. The Rule of 60 does not guarantee reversal (drop in heart scan score), nor does not achieving the targets completely destroy your chances.

We have had many people drop their scores even if they haven’t reached the targets. On the other hand, we’ve also had people who failed at first, only to see success once they achieved the 60 mg/dl targets.

But which one are you? That’s the problem. We possess limited capacity to predict who will or who will not drop their scores from the start. We know that there are factors that stack the odds in your favor (e.g., optimism, lack of Lp(a), ideal weight, vitamin D >50 ng/ml, etc.). We know that there are factors that make it tougher (overweight, Lp(a), pessimistic attitude, underappreciated hypertension, higher heart scan scores, etc.) But at the start, we just don’t know who truly needs to adhere to the Rule of 60. So we suggest that everyone, at least in the beginning, aim to achieve it.

I had an exception the other day. Rich did everything by the Track Your Plaque book. However, a starting low HDL of 27 only rose to 37 after one year of effort—way below our 60 mg/dl target. Yet a repeat heart scan showed 23% reduction.

Why would Rich be so successful despite a persistently very low HDL? There may be a number of reasons. One explanation could be that conventional measures of HDL fail to distinguish between what HDLs truly work and what do not. Look at ApoA1 Milano; remember this story? The people in the secluded mountain village of Limone-Sul-Garde in northern Italy have HDL cholesterols of 8-15 mg/dl yet do not experience excess vascular atherosclerosis, suggesting that what little HDL they have is super-effective.

Yes, large HDL seem to be more healthy and effective than small HDL, but perhaps there’s more to it. However, nobody has a HDL effectiveness test ready for us to use.

In the meantime, we continue to suggest that the Track Your Plaque Rule of 60 be considered as a means of making plaque reversal as likely as possible. You and your doctor can always adjust in future, depending on your heart scan score results.

Non-profit hospitals

Hospitals hide behind a veil of non-profit.

Ostensibly operating for the public good, most hospitals enjoy all the business advantages of non-profit status. This means that any profits that flow to the bottom line at the end of the year are not subject to tax. Hospitals point out that profit margins are modest, often ranging from 2-6%.

What they don’t tell you is that, regardless of non-profit status, lots of money can be paid out along the way. A hospital CEO who pays himself $4 million dollars a year can work for this non-profit organization. He can also direct the hospital in business expansion: pharmacies, extended-care facilities, medicine and medical supply distributorships. Your friendly hospital CEO, as well as his many administrators, can hold positions in hospital subsidiaries, complete with salaries and perks.

Yes, most hospitals are officially non-profit. But that’s a designation for tax purposes. It does not mean that hospitals are non-lucrative.

I believe that it’s time for hospitals to drop the façade of “Saint” in their names or other religious names—Methodist, Baptist, Jewish, All Saints’. More accurate would be something like “ABC Medical Enterprises, Inc.” That way, the public would be quicker to recognize that they are dealing with a business run by people eager to make more money.

Wheat five times a day

Terri couldn't understand why her weight wouldn't drop.

At 5'3", 208 lbs., she had the typical mid-abdominal excess weight that went with small LDL, low HDL, high triglycerides, a post-prandial (after-eating) fat clearance disorder, high blood sugar, increased c-reactive protein, and high blood pressure.

She claimed to have tried every diet and all had failed. So we reviewed her current "strict" diet:

"For breakfast, I had Shredded Wheat cereal in skim milk. No sugar, just some cinnamon and a little Splenda. For lunch, I had low-fat turkey breast sandwich--no mayonnaise--on whole wheat bread. For snacks, I had pretzels between breakfast and lunch, and a whole wheat bagel with nothing on it before dinner. For dinner, we had whole wheat pasta with tomato sauce and a salad. While we watched TV, I did have a couple of whole wheat crackers.

"I don't get it. I didn't butter anything, I didn't sneak any sweets, cakes, I didn't even touch cookies. And I love cookies!"

Did you see the pattern? I pointed out to Terri that what she was doing, in effect, was eating sugar 5 or more times a day. Many of her meals, of course, contained no sugar. All were low fat. But the excessive wheat content yielded quick conversion to sugar--glucose--immediately after ingestion.

Repeated surges of blood sugar like this trigger the excessive insulin response that yields low HDL, higher triglycerides, small LDL, etc., everything that Terri had.

Terri was skeptical when I suggested that she attempt an "experiment": Try a four week period of being entirely wheat-free. This meant more raw nuts and seeds, more lean proteins like low-fat yogurt and cottage cheese, chicken, fish, lean red meats, more vegetables and fruits.

After only two weeks, Terri dropped 5 1/2 lbs. She also reported that the mood swings she had suffered, afternoon sleepiness, and uncontrollable hunger pangs had all disappeared. The mental cloudiness that she had experienced chronically for years had lifted.

What happened was that the load of sugar from wheat products, followed by an insulin surge then a precipitous drop in sugar, and finally fogginess, irritability, and cravings for food all disappeared. With it, the entire panel of downstream phenomena (small LDL, CRP, etc.) all faded.

Though she started out intending to complete a four week trial, I believe that, having seen the light, she will continue to be wheat-free, or nearly so, for a lifetime.

The battle for natural hormones

The battle for preservation of availability of compounded natural hormones goes on.

It started with pharmaceutical manufacturer, Wyeth, who petitioned the FDA to disallow the mixing of pharmaceuticals, especially natural human hormones, by specially trained pharmacists at what are called "compounding pharmacies." These are pharmacies that have special equipment and where trained pharmacists can mix up specific preparations for dispensing. These are available by prescription.

For instance, I have been prescribing natural human testosterone and progesterone for nearly 10 years. I have found service to be excellent, with lots of learning materials provided to patients by the pharmacy. The pharmacists I've spoken to have been courteous and knowledgeable. Compounded hormones are also shockingly less expensive. While a testosterone patch from a pharmaceutical company costs around $4.00 per day, the same quantity of testosterone cream formulated by a compouding pharmacy costs around $0.50 per day--87.5% less.

Wyeth hides behind a smoke screen of concern over quality. But the price differences tells the entire story: they want to eliminate the inexpensive competition and hold us all hostage to the far more expensive, often inferior products that they produce. They'd sooner force a woman to use horse-derived Premarin than to allow her access to human estrogens and progesterone.

To me, this is an outrageous affront to our freedom of choice, both as consumers as well as a physician. If you feel as strongly as I do about opposing the unfair and bullying ways of Wyeth Pharmaceuticals and the FDA, the P2C2 association of compounding pharmacists makes writing a letter to your Senator easy by going to

http://iacprx.convio.net/site/PageServer?pagename=P2C2

Just enter your info and personalize the comments, and the e-mails will be generated for you.

Lipitor and memory

At first, I was skeptical. A book from a nutty author and physician named Duane Graveline kept on coming up in conversations with patients. His book, Lipitor: Thief of Memory , details his personal experience with dramatic changes in memory and thought while taking Lipitor.



Now this is a drug that I've seen used thousands of times. But I've now seen about a dozen people who have had distinct struggles with memory and clarity of thinking while taking Lipitor. Most took doses of 40 mg per day or more, though an occasional person takes as little as 10 mg. The association seems to be undeniable, since it improves after two weeks off the drug, recurs when resumed. Just today, I saw two people where this effect may be an issue.

Curiously, I've not seen it with any other statin agent. Unfortunately, uncovering any scientific data on the issue is a hopeless quest. Either it's very uncommon or, worse, the data has been suppressed.

Any way, I believe that Dr. Graveline was right: Lipitor, in a small number of people, does indeed seem to exert real detrimental effects on the mind.

If you take Lipitor, should you stop it in fear of long-term effects on your mental capacity? I think it's premature to toss the drug out based on this relatively uncommon relationship. This particular effect is likely to be idiosyncratic, i.e., peculiar to an occasional person but does not seem to apply to the majority, probably by some quirk of metabolism or penetrability of the barrier between the blood and nervous system tissue.

If, however, you feel that your thinking and memory have deteriorated on the drug, please speak to your doctor.

EKG's and heart disease


How helpful are EKG's for detecting hidden heart disease?

I pose this question because several patients asked this question just this week. It's also a frequent point of confusion and misperception.

Your EKG is nothing more than an expression of the surface electrical activity emitted by heart muscle activity. Multiple (12) leads are attached to the body simply to provide various "views" of this electical activity. EKG, or sometimes "ECG", is short for "electrocardiogram".

What modifies this surface electrical activity? Anything that modifies the electrical activity within the heart itself, or interferes with the detection of the activity. An old heart attack modifies the patterns of electrical conduction in the heart and that can change your EKG. An ongoing heart heart attack likewise. High blood pressure commonly creates changes in the EKG, as does lung disease. A bellyache can change your EKG, as can a stroke. (These non-heart-related phenomena probably are often due to changes in autonomic, or "automatic," nervous system activity.) The heart generates electrical activity in a predictable sequence that generates the heart beat, or "rhythm". EKG's are useful for monitoring heart rhythm, also.

Does having plaque in your coronary arteries have any effect on the EKG? None whatsoever, unless plaque rupture caused heart attack or is about to cause heart attack. So, you can have a horrendous CT heart scan score of, say, 3000, yet maintain a perfectly normal EKG, as long as the heart muscle is normal.

Then why bother with these iffy tests? They are indeed useful to diagnose the cause of active symptoms. For instance, go to the ER with chest pain and an EKG could show changes suggesting that the chest pain is a heart attack. EKG's are also useful for future comparison. Any change in EKG can suggest certain things, like new heart rhythm disturbances unrelated to coronary plaque.

Think of your EKG as just like buying a used car. Say I'm trying to sell you my 1999 Buick Century. It looks pretty good from the outside and I tell you that it has 70,000 miles and runs well. You ask to open the hood, look in the interior and take it out for a drive. I tell you no, you can't do that.

Would you buy the car? Of course you wouldn't. You were permitted only a very superficial examination of the car. You have no idea what's going on inside. Just because the paint job looks brand new doesn't mean the engine and transmission are good.

The same with your EKG: It's a superficial look at one aspect of this used car called your heart. If the EKG is normal, that's good, just like a good exterior on the Buick. But you cannot assume that the heart is otherwise normal.

View the EKG as a simple, superficial test that can only provide minimal reassurance, no matter how often you have it done.

A new Track Your Plaque record

Neal, a 40-year old school principal, and his young wife were terrified on learning of his CT heart scan score of 339, a concerningly high score for any age, particularly age 40.

To make matters worse, all of Neal's plaque was located in the critical left mainstem coronary artery, the shared stem of two of the three coronary arteries. A heart attack in this location is instantly fatal.

So, it was especially gratifying that Neal has set the Track Your Plaque record for largest magnitude of plaque reversal: 51% in his first year.

Studies that show a reduction in heart attack make the news. They talk about 1, 2, up to 6% regression, all achieved with high doses of statin drugs. Yet we are seeing huge, extraordinary quantities of heart disease reversal that haven't yet made headlines, amounts that far exceed those featured in the news. We should be encouraged by experiences like Neal's.

Watch for the upcoming Track Your Plaque newsletter for more details on Neal's story--how he came to the program, how he accomplished this huge effect, and why his experience was such a success. If you haven't yet subscribed, go to the www.cureality.com homepage and click on the upper right hand corner.

The Plavix Scam

Periodically, I'll see a flurry of TV ads for Plavix. It comes with a polished computer-animated cartoon that shows how platelets clump and form a blood clot, causing heart attack.

Imagine there's a pile of oil-soaked rags in a corner of your garage. I come by and tell you to get a good fire extinguisher to keep next to the rag pile in case they spontaneously ignite.

Does that make sense to you?

Wouldn't it be better to get rid of the oily rags and forget about the fire extinguisher?

Plavix is the fire extinguisher. The oil rags are your coronary plaque. The solution is to gain control over plaque behavior. Unfortunately, the TV ads (intentionally, I suspect) give the impression that blood clots just form out of the blue for no reason. Of course that's not true. It requires active, growing, inflamed atheroslcerotic plaque that ruptures, uncovering the "angry" and platelet-adhering material underneath the thin covering or endothelial lining.

Urging everybody to take Plavix is absurd. The TV ads urge many people who have no business taking the drug to take it. There are, without a doubt, groups of people who are better off taking Plavix and aspirin: people who are in the midst of heart attack, people who have unstable plaque, people with recent stents or bypass. Perhaps people at high risk for plaque rupture, e.g., extensive coronary plaque that has continued to grow.

These tactics are consistent with the experiences I've had with the sales representatives from the company (when I used to actually talk to sales reps; my office is now barred from them). The reps very aggressively would urge me to consider having everyone take Plavix. No kidding.


For us, i.e., for people who just have a heart scan score but interested in engaging in a powerful program of prevention and reversal, Plavix rarely provides any advantage. The answer is, just like our oily rag analogy, control the plaque, not put out the fire.

Lipoprotein(a) and small LDL

You won't find a lot of scientific validation for this, but it is my firm impression that small LDL, by some crazy means, has the capacity to "turn on" or "turn off" lipoprotein(a), Lp(a).

Recall that Lp(a) is a specific genetic trait, passed to us (if you have it) by mother or father. It falsely elevates LDL cholesterol and escalates heart disease risk more than just about any other known abnormality.

A frequent hint that Lp(a) might be present is a comment I hear often from patients: "My doctor said statin cholesterol drugs don't work for me. I tried them all and my cholesterol won't go down." Or, the result was substantially less than expected. That's because, when Lp(a) is lurking in your cholesterol value, it is unaffected by the statins.

It's been my in-the-trenches observation that, the more fully expressed the small LDL pattern becomes, the worse the Lp(a) behaves. In other words, if small LDL is suppressed effectively, Lp(a) doesn't seem to carry the same dangers as in someone who has plenty of small LDL. I don't know why this is. (I expect that the answer will come from someone like Dr. Marcovina at Stanford, who is at the forefront of Lp(a) structural research. Lp(a) is a complex molecule with several components. How and why it interacts with other particles remains a mystery.)

There are a little bit of data to confirm this. The Quebec Cardiovascular Study has presented some data to this effect, that the combination of small LDL particles and Lp(a) are a particularly lethal combination. We are trying to correlate our data from a CT heart score perspective to discern any statistical relationships.

This raises a very important therapeutic issue if you have Lp(a): the worst thing you can do if you have Lp(a) is become overweight. Excess abdominal fat is a huge trigger to create small LDL particles. Even though being overweight itself has no effect on the measured level of Lp(a), it activates small LDL which, in turn, throws gasoline on the Lp(a) fire.

If you have Lp(a), stay skinny.