The Track Your Plaque guide to getting grotesquely overweight

If you'd like to gain huge quantities of weight, here's a number of helpful tips:

1) Follow the advice of food manufacturers and eat the products they label "healthy", or "heart healthy", or "part of a nutritious breakfast" etc., like Shredded Wheat cereal, pretzels ("a low-fat snack"!), low- or non-fat salad dressings.

2) Cut your morning calorie intake by skipping breakfast.

3) Hang around with other heavy people. They will confirm that it's okay to be overweight.

4) Call walking your dog "exercise".

5) Get a sedentary desk job. Use your swivel desk chair to scoot about whenever possible, rather than getting up to do things.

6) Say "I've worked hard all week long. Weekends are for relaxing, not for physical activities. I deserve a rest."

7) Eat foods without thinking about it: Eat chips while watching football, eat while on the phone, daydream over the sink.

8) Eat to provide comfort when stressed.

9) Eat foods that have sentimental value, whether or not they're good for you: Freshly-baked cakes that remind you of Mom, Pop Tarts that you used to carry in your lunchbox when you were a kid, hot dogs just like Dad would buy at the baseball stadium.

10) Cut back on sleep and generate insatiable starch cravings.

11) Stack your shelves at home with great variety. That way, you'll always have something to suit your mood.

12) Say to your spouse: "It's none of your damn business what I eat! I'm a grown man/woman!" Prove it by over-indulging in obviously unhealthy foods.

13) Tell yourself that you're just too busy to pay attention to food choices. Just grab whatever you can out of a convenience store or vending machine.

See, it's easy! And that just a start.

Of course, I don't really want you to do any of these things. But if you see yourself in any of the above, and you're struggling with weight, you should seriously rethink your approach.

Your heart scan is just a "false positive"

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

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

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

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

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

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

What's better than a heart scan?


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

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

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

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

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

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

Lipids are snapshots in time; heart scans are cumulative

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

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

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

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

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

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

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

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

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

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

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

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

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





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

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

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

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

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


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

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

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

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

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

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

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

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

What role DHEA?




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

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

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



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

For instance, DHEA can:

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

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

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



The dose is best tailored to your age and blood levels. People less than 40 years old should not take DHEA. The older you are, the higher the dose, though we rarely ever have to exceed 50 mg per day. If you've never had a blood level and your doctor refuses to obtain one, 25 mg per day is a reasonable dose (10-15 mg in women 40-50 years old). It's always best to discuss your supplement use, particularly agents like DHEA, with your doctor.

Track Your Plaque Members: Stay tuned to the www.cureality.com website for a Special Report more completely detailing the hows and whys behind DHEA.

Brainwashed!

At a social gathering this weekend, as we humans like to do, someone asked me what I did for a living. I told him I was a cardiologist.

"What hospital do you work at?" he asked.

This is invariably the response I get whenever I tell people what I do. I wouldn't make much of it except that it happens just about every time.

This indicates to me just how successful hospitals, my colleagues, cardiac device manufacturers, and others supporting the status quo in heart care, have been in persuading us that the place for heart disease is the hospital--period.

Tense families, drama, high-tech...It all takes place in the hospital.

Yet the people destined to be the fodder for hospital heart care are presently well, mostly unaware of what the future holds. Also unaware that heart disease is readily, easily, inexpensively, and accurately identifiable. Ask anyone in the Track Your Plaque program who's had a CT heart scan.

We all need to rid ourselves of the idea that the hospital is the place for heart disease. If the coronary plaque behind heart attack is easy to detect and controllable, there's little or no need for the hospital for the vast majority of us.

In the majority of instances of coronary disease, the hospital should be the place for the non-compliant and the ill-informed, and not for those of us sufficiently motivated to know and do better. The formula is simple: 1) Quantify plaque with a CT heart scan, 2) Identify the causes, then 3) Correct the causes.

The Fanatic Cook: A fabulous Blog about food and nutrition

I came across this Blog authored by a nutritionist when it was highlighted on Blogger as an interesting site:

The Fanatic Cook at http://fanaticcook.blogspot.com/

I was thoroughly impressed with the insightful and entertaining commentary. I'd highly recommend this site to you for reading on nutrition. In particular, her coenzyme Q10 column was exceptionally well written and clear.(http://fanaticcook.blogspot.com/2005/02/statins-and-not-well-publicized-side.html)

Also read her column, Super NonFoods at http://fanaticcook.blogspot.com/2005/07/super-nonfoods.html.

There's also oodles of recipes, all for the taking.

Eggs: Good, bad, or indifferent?

Eggs have been in the center of the cholesterol controversy almost from the very start.

The traditional argument against eggs went that eggs, high in cholesterol (210-275 mg per egg)and with some saturated fat (1.5-2.5 grams per egg), raised blood cholesterol (and LDL). Out went the daily fried, scrambled, poached eggs that many Americans indulged in most mornings. (We replaced it with more breakfast cereals and other carbohydrate conveniences, then got enormously overweight.)





A large Harvard epidemiologic study in 1999 called this observation into question. They tracked the fate of 117,000 thousand people and then compared the rate of heart attack, death, and other cardiovascular events among various people correlated to the "dose" of eggs they ate. Egg intake varied from none to 7 or more per week. Lo and behold, people who ate more eggs appeared to not suffer more events.

This study, large and well-conducted by an internationally respected group of investigators, seem to reopen the gates for more egg consumption, though most Americans still consume eggs cautiously.

Deeper down in this study, however, was another observation: People with diabetes who ate 1 egg per day had double the risk of heart attack. Because this study was observational, no specific conclusion as to why could be drawn.

A new study conducted by a Brazilian group may shed some light. Healthy (non-diabetic) men were fed an emulsion of several eggs. Inclusion of plentiful yolks caused a dramatic slowing of fat clearance from the blood. Specifically, "chylomicron remnants" were abnormally persistent in the blood. Chylomicron remnants are potent causes of coronary plaque. (Chylomicron remnants can be measured fairly well by intermediate-density lipoprotein and VLDL by NMR, or IDL by VAP.)

Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate.

We continue to tell our patients that eating eggs in moderation is probably safe. After all, there are good things in eggs: the high protein in the egg white, lecithin in the yolk. It is the yolk's contents that are in question, not the white. Thus, you and I can eat all the egg whites (e.g., Egg Beaters) we want. It's the safety of yolks that are uncertain.

The abnormal after-eating effect suggested by the Brazilians opens up some very interesting questions and confirms that we should still be cautious in our intake of egg yolks. One yolk per day is clearly too much. What is safe? The exisitng information would suggest that, if you have diabetes, pre-diabetes, or a postprandial disorder (IDL, VLDL), you should minimize your egg yolk use, perhaps no more than 3 or so per week, preferably not all at one but spaced out to avoid the after-eating effect.

Others without postprandial disorders may safely eat more, perhaps 5 per week, but also not all at one but spaced out.

Track Your Plaque Members: Be sure to read our upcoming Special Report on Postprandial Disorders. It contains lots of info on what this important pattern is all about. Postprandial disorders are largely unexplored territory that hold great promise for tools to inhibit coronary plaque growth and drop your heart scan score. The Brazilian study is just one of many future studies that are likely to be released in future about this very fascinating area.




Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999 Apr 21;281(15):1387-94.

Cesar TB, Oliveira MR, Mesquita CH, Maranhao RC. High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. J Nutr. 2006 Apr;136(4):971-6.

Diabetes is Track Your Plaque's Kryptonite!


If there's one thing I truly fear from a heart scan score reduction/coronary plaque regression standpoint, it's diabetes.

I saw a graphic illustration of this today. Roy came into the office after his 2nd heart scan. His first scan 14 months ago showed a score of 162. Roy started out weighing well over 300 lbs and with newly-diagnosed adult diabetes.

Roy put extraordinary effort into his program. He lost nearly 70 lbs by walking; cutting processed carbohydrates, greasy foods, and slashing overall calories. His lipoproteins, disastrous in the beginning, were falling into line, though HDL was still lagging in the low 40s, as Roy remains around 60 lbs overweight, even after the initial 70 lb loss.

Unfortunately, despite the huge loss in weight, Roy remains diabetic. On a drug called Actos, which enhances sensitivity to insulin, along with vitamin D to also enhance insulin response, his blood sugars remained in the overtly diabetic range.

Roy's repeat heart scan showed a score of 482--a tripling of his original score.

Obviously, major changes in Roy's program are going to be required to keep this rate of growth from continuing. But I tell Roy's story to illustrate the frightening power of diabetes to trigger coronary plaque growth.

Like Kryptonite to Superman (remember George Reeves crumbling and falling to his knees when the bad guys got a hold of some?), diabetes is the one thing I fear greatly when it comes to reducing your heart scan score. As you see with Roy's case, diabetes can be responsible for explosive plaque growth, more than anything else I know.

The best protection from diabetes is to never get it in the first place. (See my earlier Blog, "Diabetes is a choice you make".)

What's the best lipoprotein test?

This is a frequent question from Track Your Plaque Members and others interested in improving their heart disease prevention program beyond that of simple-minded cholesterol testing.

I obtain lipoprotein testing every day on patients. I can tell you with the confidence of having done thousands of these tests that plain, old-fashioned cholesterol testing is like relying on riding a scooter to work compared to an 8-cylinder modern automobile. The scooter might get you there, but any rain, snow, or long distance to travel and you can just forget it.

All too often, lipoprotein testing uncovers abnormalities that standard cholesterol testing simply fails to uncover.

So, among the various lipoprotein tests available, which is best?


There are three commercial tests available today:

1) Gel electropheresis (GGE)--often known by its "brand" name as the Berkeley lipoprotein profile, after Berkeley HeartLabs. GGE uses a gel with an electric field applied to cause lipoproteins to migrate, based on particle size and charge.

2) Vertical auto-profile (VAP)--a form of centrifugation, or high-speed spinning of blood plasma to separate lipoprotein particles.

3) Nuclear magnetic resonance (NMR)--the idea of putting plasma in an NMR (also known as MRI) device to characterize blood proteins.

All three tests do an excellent job. All are competitively priced. All have validating data--lots of it--to justify their broad use (though health insurers, in their vast wisdom, would still have you believe that the tests are "experimental").

But is one better?

Having done many of all three (though least of VAP), I am partial to Liposcience's NMR. (By the way, I receive no fees from Liposcience to use their test, nor to promote it in any way.)

I believe NMR is superior in a few ways:

1) I believe that the LDL particle number is the best way to truly quantify LDL, better than apoprotein B and "direct" LDL.

2) It provides what I believe to be more accurate small LDL measures.

3) It provides intermediate-density lipoprotein (IDL), a post-prandial, or after-eating, measure not available on the other two.

Perhaps I'm biased because I use the NMR most frequently. But I've used it because I felt it yielded superior, more clinically believable, data.

In truth, all three laboratories do an excellent job and you'd be served fine by obtaining any of the three. But my heart goes to NMR.

Vitamin K2, aspirin, fish oil and blood thinning

An interesting question came up from one of our Track Your Plaque Members on the Forum.

"I am now taking 9 mg of vitamin K1 and 1000 mcg of K2.

Does taking this supplement with this much K1 have a counteracting effect on the thinning/anticlotting properties of aspirin and fish oil that I also take?"


Great question (along with lots of other greater discussions we have on the Forum.)

The answer: Vitamin K should have no effect on the platelet-blocking effects of aspirin or fish oil. The majority of blood clot inhibiting effects of aspirin and fish oil arise from their ability to keep blood platelets from "clumping" (just like the TV commercials for Plavix).

Vitamin K, on the other hand, participates in the liver production of blood clotting factors (like II, VII, IX, and X, among others for you curious ones).

Thus, vitamin K-dependent clotting factors and platelet-blocking are two separate pathways to forming blood clots. Some of us refer to the difference as "red clots" from the vitamin K pathway and "white clots" from the platelet pathway, since they really do have this different physical appearance.

The vitamin K2 conversation, like that about vitamin D, is fascinating for its potential to provide the missing link between the tightly-tied fortunes of bone health and atherosclerosis. Why is someone with a high CT heart scan score far more likely to have osteoporosis? Vitamin D and K2 deficiency may provide the missing link for many people.

"Drug no cure for gluttony"

That's the headline I'd like to see associated with rosiglitazone, brand name Avandia.

The recent negative press, whether deserved or not, surrounding the prescription drug rosiglitazone for pre-diabetes and diabetes highlights the fact that drugs never--never--substitute for what we can achieve with lifestyle changes.

Typically, rosiglitazone reduces blood sugar a few milligrams, reduces C-reactive protein, and very modestly reduces triglycerides and its associated evil lipoprotein friends. It also causes an average weight gain of 8 lb in the first year of use.

What will weight loss achieve, especially if accomplished through dramatic reduction or elimination of processed carbohydrates and wheat products, along with fish oil supplementation, vitamin D normalization, and exercise? Extraordinary benefits, far superior to what is achievable with this drug. In fact, while rosiglitazone is a Band-Aid for this process, the lifestyle changes can represent a cure in many or most instances.

It should come as no surprise that a drug that does nothing more than increase sensitivity to insulin cannot erase the devastating effects of an unhealthy life. Take rosiglitazone but neglect exercise, don't bother with vitamin D, indulge in pretzels and breakfast cereals, gain more weight . . . It serves the drug company's agenda better than it serves health.

Rosiglitazone not so rosy?

Dr. Steve Nissen of the Cleveland Clinic published a study that suggests that the pre-diabetes and diabetes drug, rosiglitazone, may increase likelihood of heart attack by 43%.

I say "suggests" because the analysis was something called a "meta-analysis", a re-examination of data obtained by pooling unrelated studies and reanalyzing the data. Strengths of this sort of analysis: Sometimes trends that are not evident in smaller studies finally become evident in the larger numbers of participants obtained through pooling of data. Downside: Any statistician will tell you that a meta-analysis can only suggest an association, it cannot prove it.

Nonetheless, we are talking about people's lives. As they say, if you are taking this drug, also known by the brand name, Avandia, then talk to your doctor. I think that this is sound advice, as there are a number of factors to weigh in decision making. For instance, how far along the diabetic path are you? Have you had negative experiences with other agents?

It will, unfortunately, be months to years before confirmatory evidence on this question become available. In the meantime, Nissen will accuse the drug industry of pushing drugs through the FDA approval process without full safety data. GlaxoSmithKline, the manufacturer of Avandia, will counter with claims of weak data, the existing trials not confirming Nissen's findings, etc. We've seen it before.

My take on this is to step back and look at the broad picture. Do we need yet another reason to say that it's far better to maintain normal body weight, dramatically reduce reliance on processed carbohydrates and wheat, exercise, and following other insulin-sensitizing strategies, rather than rely on insulin-sensitizing drugs? (That's what rosiglitazone is supposed to do.) Metabolic syndrome, also known as pre-diabetes, or diabetes is present to various degrees in two thirds of all adults I meet. Nearly all of it is self-inflicted. Nearly all of it is curable with the above lifestyle strategies if undertaken early enough in the process.

A 190 lb, 5 foot 2 inch woman, or a 220 lb, 5 foot 10 inch man, both of whom are surprised that they have pre-diabetes really need to get a grip on reality and health. To me, it's no surprise that drugs do not reverse all the nasty manifestations of lifestyle gone berserk. It should also come as no surprise that the complex, chaotic physiologic mess created by metabolic syndrome and pre-diabetes is not perfectly managed by adding one drug.

The lipid distorting effects of weight loss

Roger experienced a near-fatal heart attack 6 years ago. He survived thanks to the quick action of bystanders who initiated CPR and called 911. An emergency catheterization was performed and a stent implanted into the closed right coronary artery. But that's not why I tell Roger's story.

Since then, Roger has become comfortable with the idea that he has heart disease. His initial commitment to good nutrition and exercise has waned, as it often does in us distractable humans. So Roger gained about 30 lbs through a long winter, inactivity, eating frozen dinners, and the cookies and baked goodies his daughters made him.

As a result of the weight gain and inactivity, Roger's HDL dropped to 32 mg/dl, triglycerides rose to 211 mg/dl, blood sugar crept up into the pre-diabetic range of 116 mg/dl. Undoubtedly, small LDL was out of control beneath the surface. His tummy reflected the weight gain, flaccid and overhanging his belt.

I read Roger the riot act. I reminded him of what he had experienced and nearly didn't survive. Weight loss and a re-invigoration of his nutrition and exercise efforts was going to be crucial.

Roger listened and took it to heart. Over three months, he lost 24 lbs, a phenomenal result. However, his repeat lipid panel showed an HDL of 28 mg/dl, triglycerides 234 mg/dl, blood sugar unchanged.

"I don't get it! I lose all this weight and the number get worse?!" Roger was understandably upset after his enormous effort.

I told Roger that after a profound weight loss, lipids can go berserk for up to two months after weight has stabilized. Typically, HDL drops and triglycerides rise--the opposite of what we want. But wait another two or so months after weight has stabilized and the numbers begin to look beautiful.

Why does this crazy effect happen? I really don't know and I've never heard a satisfactory explanation for it. But it is very real and quite predictable.

The lesson: after a substantial weight loss, be patient. Check your lipid numbers too soon and you might be confused or disappointed. If you do check them, bear in mind that additional time may need to pass before you see the weight loss fully reflected.

Cholesterol reduction and wheat

In my previous post, Identical twins and the explosive influence of weight , we witnessed an excellent example of the profound influence of food choices and weight control on lipoproteins. The heavier twin among these 35-year old male twins (Steve) had an LDL particle number over two-fold higher than his more slender counterpart (Alfred).

The heavier twin, Steve, got here through numerous and longstanding dietary excesses: fast foods, saturated fats, sweets, processed foods. The conventional answer to Steve's lipid dilemma would be to modestly reduce his reliance on saturated fat, exercise, and limit snacks.

How far would that get Steve? Not very far at all. With regards to his high LDL particle number of 2256 nmol/l (representing an "effective" LDL cholesterol of around 225 mg/dl), it would be reduced a little, perhaps 10%.

Notice, however, that 72% of all Steve's LDL particles are small (1639/2256). This is the pattern that responds dramatically to a sharp reduction in processed carbohydrates, especially wheat-containing products.

If Steve were to eliminate all wheat products--all breads, breakfast cereals, pretzels, cookies, cakes, pasta, crackers--LDL particle number will drop dramatically, perhaps 50%, often more depending on the magnitude of weight loss. Small LDL will respond most obviously and will be sharply reduced, perhaps disappear. Incidentally, these changes might not be well reflected by the conventional calculated LDL cholesterol, since small LDL particles are well-concealed by standard measures.

Reducing corn products, white and brown rice, and potatoes would also add to the effect. But, in 2007, wheat products represent 90% of the problem for the majority of people. Reducing or eliminating wheat therefore yields the biggest effect by a long shot.

Steve therefore represents an excellent example of how reducing processed carbohydrates, esp. wheat-containing products, can yield an unexpected and paradoxical reduction in LDL cholesterol as evidenced by the highly accurate LDL particle number (or apoprotein B). Reducing saturated fat sources also helps, but it certainly will not yield the kind of results most people need. You've got to be smarter than the simple-minded conventional advice.

Identical twins and the explosive influence of weight

A Track Your Plaque member, Eugene, brought this fascinating story to my attention.

Eugene has two nephews, identical twins aged 35 years. Despite their similar personalities and appearances, somehow these two drifted apart in weight with Steve outweighing Alfred by 30 lbs.

Eugene explains:

These guy's are big not, but overly fat. Just big. One is about 30 lbs heaver than the other. They live 2 blocks apart, they ate the same (together) meal the night before the blood work. Their mother is a type 2 diabetic with a heart condition. Steve does not eat as well as his twin, junk food and a lot of processed starches.


Their results:



LDL-Particle number
Alfred 900
Steve 2256

Small LDL-P
Alfred 400
Steve 1639

HDL-C
Alfred 44
Steve 36

Triglycerides
Alfred 85
Steve 355

Metabolic Syn.
Alfred no
Steve yes


Glucose

Fasting
Alfred 93
Steve 112

1hour
Alfred 134
Steve 206

2 hour
Alfred 105
Steve 172


Identical twins begin with the very same genetic background. As these two graphically illustrate, weight can have a profound influence in the genetically susceptible.

LDL particle number alone is 250% greater in the heavier twin. The dreaded small LDL particle is over 400% worse! Look also at the dramatic differences in blood sugar.

If you ever had any doubts about the importance of excess weight and nutrition, just remind yourself of this fascinating illustration.

Thanks, Eugene.

Low-fat diets raise triglycerides

Martin, a hospital employee, knowing that I fuss a great deal with lipids and lipoproteins, showed me his lipid panel because the result triggered a "panic value" for triglycerides at 267 mg/dl. He asked if he should go on a serious low-fat diet.

I asked Martin what he had for breakfast: a whole wheat bagel with no-added-sugar jam. Lunch: a turkey sub on whole grain bread, no mayonnaise. Snacks: baked chips, pretzels ("a low-fat snack!").

In years past, if person developed high triglycerides levels, a very low-fat diet was prescribed. Someone would come to the hospital, for instance, with abdominal pain from pancreatitis (an inflamed pancreas)due to the damaging effects of triglyceride levels >1000 mg/dl. For this reason, many people still believe that all instances of elevated triglycerides should be treated with a reduction in fat intake.

This is absolutely wrong. While a fat restriction may reduce triglycerides in genetically-programmed responses when triglycerides are >1000 mg/dl, lesser levels of high triglycerides of, say 250 or 300 mg/dl, do not respond to dietary fat restrictions as a sole strategy.

Yes, a reduction in unhealthy fats (saturated, trans, polyunsaturated) helps. But a reduction in fats of all sorts is not necessary and can, in fact, worsen the problem. We learned this lesson years ago with the Ornish diet and similar ultra low-fat approaches. When you reduce fat intake significantly to <10% of calories, triglycerides go way up. In those days, it wasn't uncommon to see triglycerides skyrocket past 200 or 300 mg/dl on these diets.

Why are triglycerides important? Triglycerides are an ingredient in creating the lipoproteins VLDL, IDL, small LDL. Elevated triglycerides trigger a drop in HDL, a shift towards small, ineffective HDL, and contribute to heightened inflammation. Higher triglycerides also tend to go hand in hand with lipoproteins that persist for extended periods (12-24 hours or longer) in the blood after a meal.

Triglycerides respond very nicely to a dramatic reduction in processed carbohydrates, especially wheat and corn. Of course, wheat is the bulk of the problem, since it has grown to occupy an enormous role in many people's diet, not uncommonly eaten 3,4, or 5 times per day in various forms, as it has in Martin's diet. Eliminating all sources of high-fructose corn syrup is also helpful, since high-fructose corn syrup shoots triglycerides way up. (Recall that high-fructose corn syrup is everywhere: ketchup, beer, low-fat or non-fat salad dressings, breads, fruit drinks, sports drinks, breakfast cereals, etc.)

Curiously, it is a fat that also powerfully reduces triglycerides in the form of fish oil. In the Track Your Plaque program, fish oil, taken at truly effective doses of 4000 mg per day or more (to provide at least 1200 mg EPA+DHA), is our number one choice after reduction of processed carbohydrates for reduction of high triglycerides.

The dreaded niacin "flush"

As most anybody who takes niacin knows, it can cause a hot flushed feeling over the chest and face that is generally harmless, though quite annoying.

Many doctors are frightened by this response and will warn patients off from niacin. Some people who take niacin are so annoyed that they find it intolerable.

However, a very simple maneuver can relieve the hot flush in over 90% of instances: Drink water. Let me explain.

I usually instruct patients to take niacin at dinnertime. That way, food slows absorption modestly. I also ask them to drink water with dinner. If the flush occurs after dinner (usually 30-60 minutes later), then drinking two 8-12 oz glasses of water immediately breaks the flush within 3 minutes in the great majority of people. It's quite dramatic.

Doing this around dinner (lunch works just as well) allows sufficient time to clear the excess water from your body before bedtime and spare you the aggravation of disrupted sleep to urinate. Drinking plenty of water works most of the time. Only an occasional person will need to take a 325 mg uncoated aspirin to more fully break the flush. I generally suggest that patients keep the uncoated aspirin in reserve if the water doesn't provide relief within a few minutes.

Thankfully, the intensity of the niacin flush lessens, often disappears, with chronic use.

Why do some people develop the flush and other don't? It is believed that some people metabolize niacin more rapidly to a compound called nicotinuric acid, a niacin metabolite that causes dilation (relaxation) of skin capillaries--thus the flush. The rapidity of converting niacin to nicotinuric acid is determined genetically.

An occasional person really struggles with niacin to the point of intolerance. However, on the positive side, these people may also be "hyper-responders" to niacin, i.e., they show exagerated benefits in raising HDL, reducing small LDL, etc., from small doses such as 250 mg per day.

If you experience the hot flush of niacin, think water to put out the fire.

A cure for pessimism?

Followers of the Track Your Plaque program know that we place great value on having an optimistic outlook. Not only are you more likely to be happy and successful in life, you are also far more likely to drop your CT heart scan score. Virtually everyone who has succeeded in dropping their heart scan score dramatically has been an optimist, including our most recent record holder who dropped his score an astounding 51%.

But what if you are a pessimist, someone who gripes and complains about everything, sees the bad in other people, blames others for anything and everything that goes wrong--yet you still desire to drop your heart scan score? Are you a lost cause? Should you just give up?

I don't think so. I will admit that, of all the hurdles we encounter in trying to purposefully stop or reduce heart scan scores, overcoming a pessimistic attitude is probably the toughest. Tougher than being overweight, maybe tougher than even Lp(a).

Perhaps there's a solution in two years of psychotherapy sessions with a counselor, or exploring unresolved childhood conflicts with a psychologist, or an antidepressant drug. Pessimism is, after all, a deeply-ingrained pattern of behavior, something that can't be changed just by suggesting it or simple self-realization.

The closest thing I know of to a quick and relatively easy solution for converting a pessimist to an optimist is very simple:

Do good things for other people.

Something peculiar happens to the pessimist when he/she starts to help others. They are less threatened by other people (since much griping is really fear in disguise), begin to see others as vulnerable creatures who could use their help rather than sources of annoyance, and a kinship with others is acquired.

Doing good things can mean giving blood, donating money to the Sierra Club or other charity, volunteering with the Boy Scouts, tipping the hard working waitress trying to pay for college more generously, paying compliments to people around you, helping a neighbor carry the groceries when you see him struggling, showing a child how to make a paper airplane . . .

Good deeds can take a million different forms. But it must involve you personally. It can't mean delegating a helpful activity to your spouse. You must also do it frequently, not just once a year. It doesn't have to cost money, it doesn't have to involve a lot of time (though your personal bodily involvement does yield the greatest return in optimism). These are things anyone can do and help make the world around you a little better.

If taking these small steps towards an optimistic attitude are too much for you, then I would worry that you are destined to fail in dropping your heart scan score.