Heart Scan Curiosities #8: Fat heart

Here's a curious incidental finding on a heart scan: an unusual fat accumulation around the heart.



The arrows point to an unusually large accumulation of fat tissue on either side of the heart. This man was mildly but not excessively overweight at 5 ft 10 inches and 201 lbs.

I know of no specific implications of this curiosity. It makes me wonder if he was very obese at one time and has since lost the weight.

Chocolate and blood pressure

A recent very detailed and clean study on the effects of a small serving of dark chocolate on blood pressure was just published in the Journal of the American Medical Association.

I was going to do a little Blogging on this interesting study but I read the Fanatic Cook's wonderfully insightful comments. I'd direct you to her discussion, instead: A small daily dose of dark chocalate lowers blood pressure at http://fanaticcook.blogspot.com/. I couldn't have said it any better.

By the way, the authors of the study had no financial ties to the chocolate or cocoa industry. Refreshing.

Does prevention save money?

Prevention and reversal of heart disease are undoubtedly preferable to the current crash and repair model currently followed by doctors and hospital, the model that has created an enormous medical device industry to support it.

But does it save money? This debate often boils down to a metric of "lives saved per $100,000". Thus, the statin drugs (of course) have been subjected to such analyses and have been shown to be "cost-effective."

But how does a powerful heart disease prevention and reversal program like Track Your Plaque compare to the current crash and repair procedural approach to heart disease? This is a very difficult analysis, one that is subject to enormous variation, depending on the population studied and the prevalence of disease, the local practice habits (e.g., in the northwest Cleveland suburb of Lorain, virtually everybody going to the hospital for any heart problem gets one or several heart catheterizations), and other factors.

There's also the difficulty of what should constitute a prevention program. Is it like that used in the COURAGE Trial of "optimal medical therapy" that included nitroglycerin, aspirin, a beta blocker, and statin drug (which we regard as a laughably silly approach), or one like Track Your Plaque in which we try to correct the causes of heart disease, not just palliate (BandAid) them? Costs vary. The "optimal medical therapy" is very costly due to its reliance on medications to treat symptoms. Our program is somewhat costly because of the reliance on a CT heart scan and lipoprotein analysis (though, in the long perspective, our costs are modest).

We asked this question and came up with a lengthy analysis. Bottom line: Following the Track Your Plaque program saves enormous sums of money. Because of the complexity of the analysis, which is theoretical and not a real-world test, we confined our analysis to men in the 40-59 year old age group. If this group alone were to subscribe to a intensive but rational program of prevention like Track Your Plaque, over $20 billion dollars per year would be saved.

If the analysis were extended to women of all ages and men older than 59, the numbers would balloon to many more tens of billions of dollars. Such a savings wouldn't cure the healthcare system's growing financial crisis, but it sure would be a big help. Sort of like converting to a hydrid car--you don't eliminate the need for gas, but you'll save a lot in fuel costs.

The Track Your Plaque approach makes sense because it is, bar none, the most powerful approach to gaining hold of heart disease risk available. But it also makes sense from a financial standpoint. Now, if we can only convince the hospitals, the $30 million annual salary device manufacturer CEO, and my procedure-crazy colleagues that this way makes more sense.

Watch for our analysis on an upcoming Track Your Plaque Special Report.

Where should fiber come from?

Ray had the usual protuberant belly overhanging his beltline of someone who was over-reliant on processed starches, particularly wheat.

After all, he ran a sandwich bakery. He sheepishly admitted that he ate the products of his own production line every day while at work, even bringing a few sandwiches home.

At 5 ft 10 inches, 201 lbs, he wasn't terribly overweight, but all the excess was in his beltline. He had the lipoproteins to match: HDL 38 mg/dl, triglycerides 180 mg/dl, 83% of all LDL particles were small, excess VLDL and IDL. Blood pressure: 140/88. Blood sugar: 112 mg/dl.

With a CT heart scan score of 698, Ray had some work to do.

Among the strategies we discussed was a need to dramatically reduce, perhaps eliminate, wheat products and other high-glycemic index foods.

"You've got to be kidding me!" Besides the inconsistency with his business, he was puzzled on what foods were edible for his pattern. We discussed how he could easily replace his reliance on wheat and breads with more vegetables, more fruits, more lean proteins, and more healthy oils.

"But I won't get any fiber!" he declared. That was why he tried to choose whole wheat bread for his sandwiches.

This is a common concern when we discuss how grains, particuarly wheat, need to be sharply reduced. In the most recent edition of his Paleo Diet Newsletter, Dr. Loren Cordain has laid out a wonderful graph that beautifully illustrates the issue:




(From The Paleo Diet Newsletter at http://www.thepaleodiet.com/newsletter/back_issues.shtml)


In other words, reducing or eliminating "fiber-rich" grains and replacing their calories dramatically increases fiber content of your diet.

For Ray, whose livelihood depends on promoting and perpetuating the use of wheat breads, it will be tough to keep him on the right track. My prediction: the results he will see will be substantial and it will become difficult to return to eating his own products.

There's no doubt that this concept can be economically disruptive for many people, including Ray. It's a tough situation we've created: a huge industrial complex based on growing grains and wheat, processing it into breakfast cereals, bagels, pretzels, crackers, and sandwiches. But it has also contributed to the epidemic of obesity and the patterns that people like Ray have.

But the startling fact remains: If replaced with vegetables and fruits, reducing grains increases the fiber content of your diet, and not jsut a little bit, but enormously. If green peppers and spinach had brand names like "Fiber One" and "Smart Start" along with flashy boxes, then maybe it would be an easier concept to grasp.

To sign up for Dr. Cordain's wonderfully informative newsletter, go to http://www.thepaleodiet.com/newsletter/back_issues.shtml.

The Detection Gap

You've heard of the Generation Gap, the Income Gap, the Technology Gap, the Gender Gap, and the Achievement Gap.

How about the Detection Gap?

Haven't heard of it? That's the gap between coronary heart disease detected by conventional methods widely practiced in the community and the real prevalence of the disease.

The standard approach to coronary heart disease detection is a relatively simple formula. One of three things are sought:

1) Symptoms of heart disease like chest pain or breathlessness.
2) An abnormal EKG or abnormal stress test.
3) A catastrophe like heart attack or sudden cardiac death.

By this equation, the American Heart Association (AHA) estimates that 36% of American men and women have coronary disease.

However, we say the number is more like 48%. That's the number we arrive at when we ask: How many men and women have CT heart scan scores above zero?

The difference is the Detection Gap. Though only around 12%, it amounts to millions of people. The problem is that, by the conventional approach to detection of heart disease, you often don't know you have it until you're lying on a hospital gurney being wheeled off to a major procedure. Or your friends, family or neighbors find your body.

If heart disease is detected by a CT heart scan, it tends to be early, before catastrophe strikes. You can use tools like niacin, vitamin D, flaxseed, etc., all the components of the Track Your Plaque approach.

If heart disease is detected by waiting for the appearance of symptoms, then a stress test (usually nuclear) is followed by a heart catheterization, stents, bypass, etc. So there's more than a Detection Gap. There's also a difference in the sorts of therapies chosen. There's certainly a difference in cost.

In my view, there is no rational reason not to close the Detection Gap. While CT heart scan scores aren't perfect, they're damn close. The Detection Gap could be closed to around 2%. We'd also save billions of dollars.

Apoprotein B on VAP

We've just received an announcement that, if your Vertical Auto Profile lipoprotein test (Atherotech) is provided through the national Quest laboratories (a large national laboratory company), they will include an apoprotein B.

This represents an improvement over the previous "direct LDL," a measured LDL cholesterol. Recall that standard lipid panels obtained in hospitals and doctors' offices is a calculated LDL, based on the 40-some year old Friedewald calculation. In my view, the Friedewald calculated LDL is a dinosaur that is virtually useless and needs to be retired.

Direct, or measured, LDL is a slight improvement. It removes some of the inaccuracy introduced by the assumptions built into the calculated value.

Apoprotein B (also called apoprotein B100) is yet another improvement. Apo B's have been available for years, but was not provided on the VAP. The Atherotech people have done a good job of making VAP more broadly available through "drawing stations" and proponents like Life Extension. Adding an ApoB is a favorable development, since it incorporates the risk of other ApoB-containing particles, like VLDL, IDL, and Lp(a). Several studies like the Quebec Cardiovascular Study have shown that ApoB is a superior predictor of heart disease compared to calculated LDL.

I still believe that the gold standard for assessing risk from an LDL standpoint is the LDL particle number along with the other measures provided by the NMR assay (Liposcience). However, the addition of the ApoB to VAP adds greater confidence to the measures provided by this technique. Those of you who rely on the VAP assay provided by Quest for your Track Your Plaque program for control of CT heart scan scores therefore have access to this improved panel.

Estrogens and CT heart scan scores

A recent study from the Women's Health Initiative (WHI), the large study that originally showed no reduction in heart attack with use of estrogens in postmenopausal females, has just published a new study.

In this new effort, women who took Premarin (horse estogens) had up to 61% lower CT heart scan scores. This new study was confined to the women from the original WHI study who had entered the study between the ages of 50-59 years (average 55 years old), since this was the significant subgroup of women who actually showed a reduction in heart attack risk, whereas other groups showed no benefit or a slightly increased risk.

For a full discussion of this fascinating result, see the Track Your Plaque report, Can estrogen reduce CT heart scan scores? at http://cureality.com/library/fl_06-017estrogen.asp. (This report is open to both Track Your Plaque Members and non-Members.)

I truly wish that the issues surrounding female hormone replacement were clearer. This new perspective adds just another interesting twist on a strategy that too many people, in my view, dismissed too readily with the initial WHI results.

To add to an already confusing situation, the WHI study was sponsored by Wyeth Pharmaceuticals, the maker of Premarin, and many of the investigators participating in the study obtained financial compensation from Wyeth. On the one hand, we have to give credit to the company and the investigators for publishing the initial study that panned the effects of Premarin. On the other hand, it makes any positive data somewhat suspect, particularly since there is a far less costly and probably superior preparation called human estrogens.

Incidentally, Wyeth is also behind the maddening FDA petition to prevent "compounding" pharmacies from dispensing human hormones like estrogen unless made by a drug manufacturer. They hide behind claims of concerns over safety. Nonsense. This is pure profiteering and protection of their enormously profitable franchise and has nothing to do with public safety. If there were genuine concerns that the compounding pharmacies, around for decades with an excellent reputation, pose safety issues, why not just lobby for improved oversite?

If only we had data like WHI that used human estrogens and human progesterone. I suspect that we'd see bigger, better effects with less of the ill effects peculiar to the cross-species use of Premarin and the synethetic progestin, Provera.

The wheat-free life

"There's nothing else I can do with my diet," declared Whitney, a 53-year old university faculty member.

"I don't eat meat. I never eat fried foods. I can't remember the last time I used butter. My idea of having a treat is a handful of blueberries. What else can I do?"

Whitney was clearly frustrated. With a CT heart scan score of 264, she was worried that trouble was just around the corner. Her lipoprotein panel had demonstrated a severe small LDL pattern, with 70% of all LDL particles in the small category. HDL was also low at 41 mg/dl.

"What did you eat for breakfast?" I asked.

"Same as always: Either Fiber One cereal or Shredded Wheat. No sugar, just skim milk. Sometimes I have some orange juice, fresh-squeezed of course."

"How about lunch?"

"If I brown-bag it, I'll usually have a reduced-fat turkey breast sandwich on whole grain bread. About once a week, I'll have a whole wheat bagel--no cream cheese, of course."

"Dinner?"

"Sometimes I have chicken--skinless--with a vegetable, corn, or salad. I love pasta, but I always use whole wheat."

"How about snacks?"

"I try not to snack. But, when I'm desperate, I usually grab some Triscuits or pretzels."

The problem with Whitney's diet was clear: Too many sugar-equivalents, otherwise known as wheat. I suggested that her diet was far too heavily laden with wheat products. She seemed skeptical. "But this is as low-fat as I can get! Now you're going to take away wheat?"



What happens when you eliminate wheat from your diet?

Several predictable, consistent changes can be observed:


--HDL cholesterol goes up.

--Triglycerides go down.

--Small LDL particles are reduced.

--LDL cholesterol drops (the amount dropped depends on the proportion of small LDL pattern)

--Blood sugar drops.

--Blood pressure drops.

--C-reactive protein (an index of imperceptible inflammation) drops.


In addition to these measurable changes, several perceptible improvements often develop: more energy, less afternoon "slump," better sleep, sometimes less rashes.

Since Whitney was skeptical, I suggested a simple 4 week "experiment": Eliminate wheat products entirely for 4 weeks and see for herself what happens. I also warned her that, while I believe that elimination of wheat is a great strategy, she could negate the benefits by indulging in candy, soft drinks, and other junk products. It would therefore be necessary to maintain an otherwise healthy diet.

So Whitney gave it a try for 4 weeks. To make up for the dropped calories, she increased her reliance on vegetables, fruits, lean proteins, nuts, seeds, and healthy oils.

After losing 6 lbs over the 4 weeks without otherwise trying, she was convinced. She was further convinced when we reassessed her laboratory work: HDL went up 10 mg/dl; triglycerides down 120 mg/dl; blood sugar dropped from 112 mg/dl (pre-diabetic) to 95 mg/dl (normal). Several months later, we checked her lipoproteins. Small LDL had dropped to around 30% of total LDL--a big improvement.

It's contrary to conventional wisdom. It's counter to the USDA Food Pyramid. It's certainly not what the American Heart Association says. It could potentially disrupt the economics and politics of the enormously powerful food industry.

But, more often than not, the results are impressive to phenomenal.

Death of a $7 billion industry

Vitamin D has taken its place as a crucial ingredient for coronary plaque control and control of CT heart scan scores.

Vitamin D replacement is also crucial for bone health, particularly the prevention of osteoporosis. But conversations about vitamin D replacement to true healthy levels is notably absent from the conversation on treatment and prevention of osteoporosis. Yes, you will find a small dose of vitamin D in calcium tablets and in multivitamins. Those of us who check blood levels of 25-OH-vitamin D3 in patients will tell you: They don't work. These are unabsorbable forms of vitamin D and at trivial doses. There was an attempt to give this issue a little cursory attention when a small dose of vitamin D was added to Fosamax (Fosamax D).

There are an estimated 50 million Americans with various degrees of osteoporosis. It's numbers like this that make the drug manufacturers salivate. Osteoporosis treatment is also chronic. This is among the holy grails of the drug industry: developing agents for widespread ailments that require long-term treatment that extends over years. That's a lot more profitable than 10 days of antibiotics that are over and done with in one treament course.

The osteoporosis market now stands at $7 billion per year and is expected to grow 6-7% per year, according to industry analysts. Drugs like Fosamax, Evista, and Actonel will eventually be replaced by Boniva, Eclasta, and bazedoxifene, and later by AMG-172 and balicatib. Monthly costs for these drugs can be $70 or more per month, sometimes several hundred dollars. (Experience has shown that the introduction of new drugs does not necessarily mean that other drugs will drop in price.)

Here's a clinical trial I'd like to see performed: Vitamin D restored to healthy levels of 50-100 ng/ml over an extended period and compared to a group treated with placebo. My prediction is that there will be dramatic differences in bone density. (Small studies have been performed, but no large, long-term trials of the sort that would yield real firepower.) Or, how about vitamin D to true therapeutic levels over 5 years compared head-to-head with one of the drugs. My prediction: little difference.

Vitamin D also provides an enormous panel of health benefits beyond restoration of bone density, like rise in HDL, drop in triglycerides, facilitation of control over CT heart scan scores, drop in fracture risk, drop in blood pressure and C-reactive protein, reduction in risk for colon, prostate, and breast cancer. None of the drugs can hope to provide any of these effects, except a drop in fracture risk.

Vitamin D usually costs around $2 per month. I doubt that such trials will be performed. If I were a manufacturer of osteoporosis drugs and my career success was dependent on the increasing revenues of these drugs, I would be quaking in my shoes, hoping that the public does not learn what a powerful tool good old vitamin D is. But if you are an individual just looking for health tools, vitamin D is, in my view, amongst the most powerful natural, nutritional tools you have available with outsized health benefits.

Lose weight and HDL goes . . . down

Steve started with a miserable HDL cholesterol of 27 mg/dl. As expected, the low HDL was associated with all its evil friends: small LDL, deficiency of healthy, large HDL, high triglycerides, VLDL, and a pre-diabetic blood sugar.

Steve committed to a strict diet of reduced processed carbohydrates like wheat products, reduced meat and saturated fats. He relied on vegetables, fruit, lean proteins, and healthy oils. Over a 6 month period, he lost an impressive 39 lbs. He proclaimed that he hadn't felt this good in 30 years.

We rechecked his HDL: 25 mg/dl.

"I don't get it!" Steve declared, understandably.

There's a curious phenomenon with HDL. If you lose weight, HDL goes up--but not right away. Steve had lost a substantial quantity of weight and was continuing to lose weight when the blood work was obtained. While HDL does indeed rise with weight loss, it doesn't do so immediately. In fact, in the first two or so months after significant weight lost, HDL goes down.

Why? I don't really have an explanation, but it is a very consistent effect.

Losing weight towards ideal weight is truly an effective strategy for raising HDL. But we need to be patient. If you've lost many pounds like Steve did, then waiting at least two months after weight has stabilized may be necessary to fully gauge the effect on raising HDL.
All posts by william-davis

Who knows what

You know that cynical old saying:


It’s not what you know, it’s who you know.

In other words, knowing the right person provides you strategic advantage in business, social advancement, etc.

In health, it was often true. Knowing who the better doctors were, for instance, in your city might provide you with access to better care.

Enter the Information Age. You now have access to medical information equal to that of your doctor. You now have access to patient discussions about doctors, their practices, their performance records. There is now a depth and breadth of information on health that was never available before.

I’d therefore turn the old saying into the new Health 2.0 version:


It’s not who you know, it’s what you know.


In health, information now reigns supreme, not knowing somebody else who has the right connections.

Positive: Everybody now theoretically has access to an equal amount of information, since you can access information on any topic just as easily as I can.

Negative: It puts more of the burden on you. If you screw up in health, perhaps you didn’t try to get the best information hard enough.

I love this new development, this emergence of empowerment in health. I call it self-directed health, the individual capacity to exert enormous influence over the quality of your healthcare.

This is obviously a work in progress. All the answers and tools for self-directed care, self-empowerment are not yet available, some haven’t even yet been imagined.

But they are coming.

“Too many false positives”

“Do you really think I need a heart scan?” asked Terry.

“My doctor said that heart scans show too many false positives. He says that many people end up getting unnecessary heart catheterizations because of them.”

At age 56, Terry was becoming increasingly frightened. His father had suffered his first heart attack at age 53, Terry’s paternal uncle had a heart attack at age 56, his paternal grandfather a heart attack at age 50.

Is this true? Do heart scans yield too many false positives, meaning abnormal results when there really is no abnormality?

No, it is not. What Terry’s doctor is referring to is the fact that, in the decades-long process that leads to heart attack, heart scans have the ability to detect early phases of developing coronary atherosclerotic plaque.

Let’s take Terry’s case, for example. Given his family history, it is quite likely that he does indeed have coronary atherosclerotic plaque. Will it be detectable by performing a stress test? Probably not. In fact, Terry jogs and feels well while doing so. While a stress test abnormality that fails to reach conscious perception is possible, it’s fairly unlikely given his exercise routine.

Will Terry’s coronary atherosclerotic plaque be detectable by heart catheterization? Very likely. But why perform an invasive hospital procedure just as a screening test? Should a woman wishing to undergo a screening test for breast cancer undergo breast removal? Of course not.

Is waiting for symptoms a rational way to approach diagnosis of heart disease? Well, when symptoms appear, it means that coronary blood flow is reduced. Stents and bypass surgery may be indicated. The risk of heart attack and death skyrocket. Sudden death becomes a real possibility.

In the 30 or so years required to establish sufficient coronary plaque to permit the appearance of symptoms or the development of an abnormality detectable by stress testing, there were many years when the disease was early--too early to generate symptoms, too early to be detectable by stress testing.

That’s when heart scans uncover evidence for silent coronary atherosclerotic plaque.

Should we call this a “false positive” just because it doesn’t also correlate with “need” for a catheterization, stent, bypass operation or result in heart attack within the next few weeks?

The detection of early plaque is just that: early disease detection.

Imagine, for instance, that the breast cancer that will grow into a palpable nodule or mass detectable by mammogram is detectable by a special breast scan 15 years before it becomes a full-blown tumor, metastasizing to other organs. What if effective means to halt that earliest evidence of cancer could put a stop to this devastating disease decades ahead of danger? Is this a “false positive” too?

In my view, this is the knuckleheaded thinking of the conventional practitioner: “Don’t bother me until you’re really sick.” Prevention is a practice that has become fashionable only because of the push of the drug industry. Nutrition is an afterthought, a message conceived through consensus of “experts” with suspect motivations and allegiances.

So, no, heart scans do not uncover “false positives.” They uncover early disease--true positives--years before it is detectable by standard tests or by the appearance of catastrophe. But that is the whole point: Early detection means getting a head start on prevention.

Do heart scans lead to unnecessary heart catheterizations? Yes, sadly they do. But not because heart scans are false positive. It happens because of unscrupulous or ignorant cardiologists who use the information wrongly. In my view, heart scans should NEVER lead directly to heart catheterization in an asymptomatic patient. Heart scans, as helpful as they are, do not modify the standard reasons for performing heart procedures.

If a car mechanic is dishonest and fixes a carburetor that didn't need fixing, should we condemn all car mechanics? No, of course not. We only need to develop the means to weed out the bad apples. The same applies to heart scans.

Triglycerides divided by five

Here's a bit of lipid tedium that might nonetheless help you one day decipher the meaning of shifts in your cholesterol panel.

Recall from prior discussions that conventional LDL cholesterol is a calculated value. Contrary to popular opinion, LDL is usually not measured, but calculated from the Friedewald equation:

LDL cholesterol = Total cholesterol - HDL cholesterol - triglycerides/5

For the sake of simplicity, let's call total cholesterol TC; HDL cholesterol HDL, and triglycerides TG.

We've also talked in past how a low HDL makes calculated LDL inaccurate, sometimes wildly so. (See Low HDL makes Dr. Friedewald a liar.)

Here's yet another source of inaccuracy of the Friedewald-calculated LDL: any increase in triglycerides.

Let's say, for instance, that starting lipid panel shows:

TC 170 mg/dl
LDL 100 mg/dl
HDL 50 mg/dl
TG 100 mg/dl



You're advised to follow a standard low-fat, whole grain-rich diet advocated by "official" agencies (the diet I bash as knuckleheaded). Another panel a few months later shows:

TC 230 mg/dl
LDL 140 mg/dl
HDL 50 mg/dl
TG 200 mg/dl



(Obviously, I've oversimplified the response for the sake of argument. HDL would likely go down, LDL would change more depending on body weight, small LDL tendencies, and other factors. You'd also likely get fat.)

Now your doctor declares that your LDL has gone up and you "need" a statin agent.

Nonsense, absolute nonsense.

What has really happened is that the increased dietary intake of wheat and other "healthy whole-grain foods" has caused triglycerides to skyrocket. LDL increases, in turn, by a factor of TG/5, or 40 mg/dl. Thus, LDL has been inflated by the triglyceride-raising effect of whole grains.

This is yet another reason why the standard lipid panel, full of hazards and landmines, needs to be abandoned. But calculated LDL in particular is an exercise in frustration.

Though the example used is hypothetical, I've witnessed this effect thousands of times. I've also seen many people placed on statin drugs unnecessarily, due to the appearance of a high LDL cholesterol that really represented increased TG/5, usually induced by an excessive carbohydrate intake, including those commonly misrepresented as healthy such as whole grains.

Who reads The Heart Scan Blog?

In the Heart Scan Blog, I am often guilty of speaking out loud of my varied thoughts on this crazy thing that we've created called the cardiovascular healthcare machine. But I discuss it in the context of asking "How could this be done better--better outcomes, more patient-friendly, more accessible . . . more do-it-yourself?

The last part is the part that throws most people. Do-it-yourself? My colleagues would claim I'm nuts, suggesting that coronary heart disease is something manageable by yourself. In the conventional pathway, after all, coronary disease is that unpredictable, poorly detected by standard tests, condition that then leads to heart catheterization, stents, bypass , and the like.

Several factors distinguish the readers of The Heart Scan Blog that surprised me:

--Nearly 60% are women
--There are a disproportionate number of Asian people. (Can someone explain this to me?)
--A great number have graduate degrees

I believe this tells me that The Heart Scan Blog appeals to a somewhat more sophisticated audience. This, to some degree, warms my heart, since it means that I've captured the attention of some people who may be more discriminating and thoughtful in their Internet surfing.

However, I also lament the fact that these conversations are not achieving the mainstream. After all,

Kitchen sink approach for Lp(a)


Lipoprotein(a), Lp(a), can be a tough nut to crack.

Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern.

I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people.

Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others.

Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a).

Even with this multi-agent approach, not everybody gains control over Lp(a).

That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).

While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on.

Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency.

There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years.

Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.

Making Dr. Friedewald an honest man

Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L.

Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)

In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day.

By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.

So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc.

Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction.

Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number.

It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.

The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug.

As I've warned many times before: Beware the Friedewald calculated LDL.

Some basic vitamin D issues

The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health.

Anne said:

I think it is important to stress that vitamin D supplementation needs to be continued long term.

I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times.


Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking?

If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life.


Twinb asked:

How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?

We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level.


Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level.


Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests?

Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute.


Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)

Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.

“How much vitamin D should I take?”

It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong.

The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”

Utter nonsense.

The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach.

Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child.

It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors.

It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place.

As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized.

Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t.

Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.)

With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody.

Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved.

Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined.

But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)

Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized.

There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level.

Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period.

Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it.

I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor.

If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.)

So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)

You probably don't take enough fish oil

The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:


Zero--I don't take any
17 (7%) of respondents

Less than 1000 mg per day
24 (10%) of respondents

1000-2000 mg per day
91 (38%) of respondents

2000-3000 mg per day
44 (18%) of respondents

3000-4000 mg per day
40 (16%) of respondents

More than 4000 mg per day
20 (8%) of respondents



Based on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more.

Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans.

But what dose is sufficient? What dose is ideal?

Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.)

If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary.

But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque?

This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:

--The Inuits (aka Eskimos) of Greenland and northern Canada
--The Japanese
--The Bantus of Tanzania who live along Nyasa Lake

All three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)).

The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids.

I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change.

We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change.

As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.

Vitamin D and HDL

Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies


At first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduce
processed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL.

Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke.

Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so.

Add niacin, HDL increases another 5-10 mg/dl.

Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great.

Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl.

The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl.

Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude.

Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation.

Why? How?

That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.

An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years?

Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)