Beating the Heart Association diet is child's play



In response to the Heart Scan Blog post, Post-Traumatic Grain Disorder, Anne commented:


While on the American Heart Association diet my lipids peaked in 2003. I even tried the Ornish diet for a short time, but found it impossible.

Total Cholesterol: 201
Triglycerides: 263
HDL: 62
LDL: 86

After I stopped eating gluten (I am very sensitive), my lipid panel improved slightly. This past year I started eating to keep my blood sugar under control by eliminating sugars and other grains. Now this is my most recent lab:

Total Cholesterol: 162
Triglycerides: 80
HDL: 71
LDL: 75


Isn't that great? This is precisely what I see in practice: Elimination of wheat and sugars yields dramatic effects on basic lipids, especially reductions in triglycerides of up to several hundred milligrams, increased HDL, reduced LDL.

Beneath the surface, the effects are even more dramatic: reductions or elimination of small LDL particles, reduction or elimination of triglyceride-containing lipoproteins, elimination of the marker for abnormal post-prandial (after-eating) lipoproteins, IDL, reduced c-reactive protein. Add weight loss from abdominal fat stores and reduced blood pressure.

In fact, I would go so far as to speculate that, if the entire nation were to follow Anne's lead and eliminate wheat and sugars, "need" for 30% of all prescription medications would disappear. The incidence of diabetes would be slashed, the U.S. would no longer lead the world in obesity.

Anne and I are not the first to make this observation. It has also been made in several studies, such as:

The Duke University study of low-carbohydrate diets in type II diabetics. In this study, 50% of low-carb participants became non-diabetic: They were cured.

One of the many studies conducted by University of Connecticut's Dr. Jeff Volek, demonstrating dramatic improvement in glucose, insulin (reduced 50%) and insulin responses, and lipids.

Dr. Ron Krauss' early studies that hinted at this effect, even though the "high-fat" diet wasn't really low-carbohydrate.

If wheat and sugar elimination has been shown to achieve all these fabulous benefits, why hasn't the American Heart Association spoken in favor of this dietary approach and other- low-carbohydrate diets ? Why does the American Heart Association maintain its "Check-Mark" stamp of approval on Cocoa Puffs and Count Chocula cereals?

Victim of Post-Traumatic Grain Disorder

Heart Scan Blog reader, Mike, shared his story with me. He was kind enough to allow me to reprint it here (edited slightly for brevity).



Dr. Davis,

I was much intrigued to stumble onto your blog. Heart disease, nutrition, and wellness are critically important to me, because I’m a type 2 diabetic. I’m 53 and was diagnosed as diabetic about 5 years ago, though I suspect I was either diabetic or pre-diabetic 5 years before that. Even in a metropolitan area it's next-to-impossible to find doctors sympathetic to any approach beyond the standard get-the-A1c-below 6.5, get LDL <100, get your weight and blood pressure normal, and take metformin and statins.

I’m about 5’10-and-a-half and when I was young I had to stuff myself to keep weight on; it was an effort to get to 150 pounds, and as a young man, 165 was the holy grail for me. I always felt I’d look better with an extra 10-15 pounds.
I ate whatever I wanted, mostly junk, I guess, in my younger years.

When I hit about age 35, I put on 30 pounds seemingly overnight. As I moved toward middle age I became concerned with the issue of heart health, and around that time Dr. Ornish came out with his stuff. I was impressed that he’d done a
study that supposedly showed measurable decrease in atherosclerotic plaque, and had published the results of his research in peer-reviewed journals. It looked to me as though he had the evidence; who could argue with that? I tried his plan on and off, but as so many people note, an almost-vegan diet is really tough. It was for me, and I could never do it for any length of time. But given that the “evidence” said that I should, I kept trying, and kept beating up on myself when I failed. And I kept gaining weight. I got to almost 200 pounds by the time I was 40 and have a strong suspicion that that’s what caused my blood sugar to go awry, but my doctor at the time never checked my blood sugar, and as a relatively young and healthy man, I never went in very often.

I’ve had bouts of PSVT [paroxysmal supraventricular tachycardia, a rapid heart rhythm] every now and again since I was 12 or so. I used to convert the rhythm with Valsalva, but as I moved into my forties, occasionally my blood pressure would be elevated and it made me nervous to do the procedure because it was my understanding that it spikes your blood pressure when you do it. So I began going to the ER to have the rhythm converted, which they do quite easily with adenosine. On one of my infrequent runs to the ER to get a bout of PSVT converted, they discovered my blood glucose was 500 mg/dL, and I’d never experienced any symptoms! They put me in the hospital and gave me a shot of insulin, got it town to 80 mg/dL easily,
diagnosed me as diabetic, and put me on 500 mg. metformin a day.

I was able to get my A1c down to 7, then down to 6.6, and about that time I read a number of Dr. Agatston’s books, and began following the diet, and pretty quickly got my A1c down to 6.2, and my weight down, easily, to 158. That was fine with my doctor; he acted as though I was in good shape with those numbers. Soon I ran into Dr. Bernstein’s material, and came face to face with a body of research that suggested I needed to get the A1c down to below 5! That was both discouraging and inspiring, and frankly it’s been difficult for me to eat as lo-carb as I appear to need to, so I swing back and forth between 6.2 and 6.6. I know I need to work harder, be more diligent in my carb control, and I see with my meter that if I eat low-carb I have great postprandial and fasting blood sugars, but since I don’t particularly get any support or encouragement from
either my doctor or my wife for being so “radical,” it’s hard to pass the carbs by.

One thing that always confused me was that though I saw on my meter that BG [blood glucose] readings were better with a lo-carb diet, and though I saw the preliminary research suggesting that lo-carb could be beneficial in controlling CVD, I didn’t understand why Ornish had peer-reviewed research demonstrating reversal of atherosclerosis on a very-lowfat diet. How could two opposing approaches both help? I wondered if it were possible that one diet is good for diabetes, and the
other good for heart health. That would mean diabetics are screwed, because they always seem to end up with heart disease.

From time to time I’d look for material that explained this seeming contradiction. I was determined to try to stay lo-carb, simply because I saw how much better my blood sugars are when I eat lo-carb; but it’s hard in the face of this or that website that tells you about all the dangers of a lo-carb diet and that touts the lo-fat approach. That tends to be the conventional wisdom anyway.

Finally in one of those searches I came across your material, and saw you offer what was at last an explanation of what Ornish had discovered--it wasn’t a reversal of atherosclerotic plaques he was seeing; it was that his diet was improving endothelial dysfunction in people who had had high fat intakes.

Odd as it may seem to you, that little factlet has been enough to allow me to discard entirely the lingering ghost of a suspicion that I ought to be eating very-lowfat. In fact, I was very excited to see your claim that your approach can reverse atherosclerotic plaque.

It would be nice to find a doctor who’d be supportive of your approach. My doctor isn’t much interested in diet or
nutrition. He just wants my weight in the acceptable range, my blood pressure good, and my LDL 100 or below (which I know isn’t low enough). He’s not particularly interested in getting a detailed lipid report. I hope I can talk him into ordering one so that it’s more likely I can get it covered by my insurance.

I very much appreciated the links you gave to Jenny’s diabetes websites, and I’ve resolved to get even better control of my BG by being more diligent with my diet. I’m planning on joining your site, reading your book, and following your advice. I just have this sort of deflating feeling that it would have been better if I’d stumbled upon this before I had diabetes. Still, it’s nice to have a site that offers to laypeople the best knowledge available concerning how to take care of their heart.



Mike is yet another "victim" of the "eat healthy whole grains" national insanity, the Post-Traumatic Grain Disorder, or PTGD. The low-fat dietary mistake has left many victims in its wake, having to deal with the aftermath of corrupt high-carbohydrate diets: diabetes, heart disease, and obesity.

We should all hope and pray that "low-fat, eat healthy whole grains" goes the way of Detroit gas guzzlers and sub-prime mortgages.

Drug industry "Deep Throat"

A Heart Scan Blog reader brought the following letter from a former pharmaceutical sales representative to congress to my attention.

Interesting excerpts:

As a former drug representative for Eli Lilly, I spent 20 months increasing the market share of my company’s drugs. I was recruited fresh from college with an eager desire to employ my degree in molecular biology and biochemistry. Shortly after my hiring, it became clearly apparent that a drug sale had much more to do with establishing personal relationships than it did with understanding the latest science. However, any doubts I held regarding the effectiveness of such methods were dispelled by the results of my persuasiveness and the financial rewards I received for my efforts. The latter also helped me rationalize the many ethically dubious situations I routinely encountered in my work. Upon my departure from the industry, I began working for the public’s health. Seven years later, as a result of my experiences and education I am more convinced than ever that the goals of the pharmaceutical industry often stand in direct conflict with the practice of ethical and responsible medicine. Nothing in my recent research causes me to believe that my experiences were anything but typical of the training and practice of the majority of drug reps plying their trade today.


“There’s a big bucket of money sitting in every [doctor’s] office.” – Michael Zubillaga, Astra Zeneca Regional Sales Director, Oncology


The majority of drug reps entering the work force today are young and attractive. The ranks of reps are replete with sexual icons: former cheerleaders, ex-military, models, athletes. Of course, as a sales job, the reps must be eloquent and convincing. Depending on the population, certain ethnicities are preferred either to make the rep distinct among other reps or to provide them with a cultural advantage in connecting with their clients. Noticeably lacking among most new reps is any significant scientific understanding. My personal case illustrates this point rather vividly: In my training class for Eli Lilly's elite neuroscience division, selling two products that constituted over 50% of the company's profits at the time, none of my 21 classmates nor our two trainers had any college level scientific education. In fact, that first day of training, I taught my class and my instructors the very basic but crucial process by which two nerve cells communicate with one another. It is very likely that the majority of my class couldn't explain the difference between a neuron and a neutron prior to sales school. While it's certainly a bonus to have a scientifically educated representative, it is far from a primary recruitment criterion. Youth is a much higher criterion for the sales position.

Sales representative trainers are almost always veteran sales representatives and consequently, much of the training they offer is implicit in the anecdotes they give. This informal training parallels the standard training offered by the industry and in many ways compliments it. It is tacitly accepted by management and perceived as the "real" training by many veteran sale representatives. Among the more dubious "unofficial" lessons a new rep learns are: how to manipulate an expense report to exceed the spending limit for important clients, how to use free samples to leverage sales, how to use friendship to foster an implied "quid pro quo" relationship, the importance of sexual tension, and how to maneuver yourself to becoming a necessity to an office or clinic.

The most troubling aspect of pharmaceutical sales is systematic befriending of our clients. In addition to the psychological profiling mentioned above, drug reps are taught to constantly be on the lookout for personal effects that will help us connect to our doctors. When entering an office for the first time, we nonchalantly survey it for clues to ingratiate ourselves with our client. Similarly, conversations are intentionally steered into the realm of personal details such as religion, family, or hobbies to acquire similar information. As a matter of training, we collect this data subtly. In the course of a conversation with clients, we may glean facts about their prescribing preferences, the dates of their children’s birthdays, where they were born, or what music they enjoy. Training encourages us to commit these details to memory just long enough to return to our cars and instantly type up a “call report” listing the details of our conversation. On a daily basis, we connect our computers to a central database that uploads the information we’ve acquired, allowing us to share it with our partner drug reps and company marketers. Subsequently, drug reps interweave pieces of conversation specifically tailored to appeal to their client drawn from personal information that wasn’t necessarily shared with them. For example, Dr. Jones will be nothing but grateful when I supply him with a cake celebrating his children’s birthday when, in fact, he told my partner (and not me) the birthdates several months prior in a personal conversation.


The writer's comments ring true: The relentless attention-grab of sales representatives, using clever tactics that include access to detailed records of physician prescribing habits, big smiles and eye-winking, are detailed perfectly.

There's nothing wrong with a business doing its job by marketing its products and services. What is so wrong about this picture is that one side is so well-equipped, heavily funded, with access to extraordinary resources that the other side (physicians) don't have. And the physicians aren't the victims--YOU are.

A middle-aged, receding hairline physician, faced with a 28-year old attractive woman asking all manner of ingratiating questions but knowing full well what she is doing, having strategized for weeks on how to manipulate the behavior of her "mark," is helpless.

Like the mortgage-backed security crisis, we've reached another phenomenon of crisis proportions. Direct-to-consumer drug advertising, drugs for non-conditions and well people, pinpoint marketing of drugs to physicians--it's all gone too far.

Personally, drug representatives are not welcome in my office. This generally prompts puzzled, followed by angry, looks from the representatives, often traveling with a district supervisor hoping to help polish their pitch. If patients didn't request free samples, the reps would not step foot in the office.

Triglyceride Buster-Update

In the last Heart Scan Blog post, I described Daniel's experience reducing his triglycerides from 3100 mg/dl to around 1100 mg/dl with use of omega-3 fatty acids from fish oil, along with modifications in his diet. This was accomplished in the space of around two weeks.

An update: Daniel has continued another 10 days on his fish oil, along with elimination of wheat, cornstarch, and sugars.

Repeat triglyceride: 202 mg/dl. That's 93.5% reduction in the space of three weeks--no drugs involved.

Daniel really did nothing extraordinary. He simply followed the simple advice I provided to take a moderate dose of EPA+DHA from over-the-counter fish oil supplements, along with elimination of the foods that are extravagant triggers of triglycerides.

He's got just a little further to go to achieve the biologically ideal level of less than 60 mg/dl. You can see that it is not really that difficult--provided someone didn't load you down with nonsense about "cutting your fat," or statin or fibrate drugs.

Triglyceride buster

Two weeks ago, Daniel started with a triglyceride level of 3100 mg/dl, a dangerous level that had potential to damage his pancreas. The inflammatory injury incurred could leave him with type I diabetes and inability to digest foods, since the insulin-producing capacity and the enzyme producing capacity of the pancreas are lost.

Daniel added 3600 mg of omega-3s per day. Within 10 days, his triglycerides dropped nearly 2000 mg to just over 1100 mg/dl--still too high, but an incredible start.

The power of omega-3 fatty acids from fish oil to reduce triglycerides is illustrated most graphically by people with a condition called "familial hypertriglyceridemia" that is responsible for triglyceride levels of 500, 1000, even several thousand milligrams. That's what Daniel has. Given appropriate doses of omega-3s, triglycerides drop hundreds, even thousands, of milligrams.

No question: Omega-3 fatty acids from fish oil are the best tool available for reduction of triglycerides. The effect is dose-dependent, i.e., the more you take, the greater the triglyceride reduction.

How omega-3s exerts this effect is unclear, though there is evidence to suggest that omega-3s suppress several nuclear receptors involved in triglyceride (VLDL) production and increase the expression or activity of the enzyme lipoprotein lipase, an enzyme that clears triglycerides from the blood.

I am continually surprised at the number of people with high triglycerides who are still treated with a fibrate drug, like Tricor, or a statin drug, when fish oil--widely available, essentially free of side-effects, with a proven cardiovascular risk-reducing track record--should clearly be the first choice by a long stretch.

Among its many benefits, omega-3 fatty acids from fish oil also:

Reduce matrix metalloproteinases (MMP)--Two fractions of MMPs, MMP-2 and MMP-9, are inflammatory enzymes present in atherosclerotic plaque that are suspected to trigger plaque "rupture." Omega-3s have been shown to reduce both forms of MMP.

Block uptake of lipids in the artery wall--Suggested by a study in mice.

Modify postprandial responses--In the first few hours after eating (the "postprandial" period), a flood of digestive byproducts of a meal are present in the bloodstream. While research exploring postprandial effects is still in its infancy, it is clear that omega-3 fatty acids have the capacity to favorably modify postprandial patterns. One common surrogate measure for postprandial abnormalities is intermediate-density lipoprotein, or IDL, that we obtain in fasting blood through lipoprotein panels like NMR and VAP. With sufficient omega-3s alone, IDL is completely eliminated.

Unfortunately, most of my colleagues, if they even think to use omega-3s, choose to use the prescription form, Lovaza. Indeed, several representatives from AstraZeneca, the pharmaceutical outfit now distributing this miserably overpriced product, frequently barge their way into my office poking fun at our use of nutritional supplements instead of the prescription Lovaza. "But insurance covers it in most cases!" they plead. "And your patients will know that they're getting the real product, not some fake. And they'll have to take fewer capsules!"

I never use Lovaza to reduce triglycerides, even in familial hypertriglyceridemia--the FDA-approved indication for Lovaza--and have not yet seen any failures, only successes.

Newsweek, Time, and other fronts for the drug industry

I used to believe that conventional print media--newspapers, magazines--were unbiased, untouchable flames of truth. Perhaps there was a time when this was true, when the young reporter, eager to change the world, uncovered the story that righted some huge wrong.

Those days are drawing to a close.

Today, the once powerful print media are collapsing due to the competition of the cheaper, broader reach of the internet.

Jogging does NOT cause heart disease


Periodically, I'll come across a knuckleheaded report like this one from Minneapolis:

Marathon Man’s Heart Damaged by Running?


Of course, the obligatory story about how a cardiologist came to the rescue and "saved his life" with a stent follows. In other words, a stent purportedly saved the life of this vigorous man with no symptoms and high capacity for exercise.

Does vigorous exercise, whether it's marathon running, long-distance biking, or triathlons, cause coronary disease? Should all vigorous athletes run to their doctor to see if they, too, need their lives to be "saved."

Let me tell you what's really going on here. People with the genetic pattern lipoprotein(a), or Lp(a), tend to be slender, intelligent and athletic. For genetic reasons, these people gravitate towards endurance sports like long-distance running. Lp(a) is a high-risk factor for coronary disease. It is the abnormality present in the majority of slender, healthy people who are shocked when they receive a high heart scan score or have a heart attack or receive a stent. (I call Lp(a) "the most aggressive known coronary risk factor that nobody's heard about.")

The association between endurance exercise and heart disease is just that: an association. It does not mean that exercise is causal. Having seen coronary plaque detected with heart scans in many runners, virtually all of whom demonstrated increased Lp(a), I believe that Lp(a) is causal.

Unfortunately, the man in the Minneapolis story, now that his life is "saved," will likely be advised to take a statin drug and follow a low-fat diet . . . you know, the diet that increases Lp(a).

Warning: Your pharmacist may be hazardous to your health

Pharmacists can be very helpful resources when it comes to questions about prescription drugs.

The operant word here is drugs.

What they are most definitely not expert on are nutritional supplements. In fact, a day doesn't pass by without having to dispell one falsehood or another conveyed to a patient about a nutritional supplement by a pharmacist.

Among the more common falsehoods told to patients by pharmacists:

"You have to take Niaspan. Sloniacin doesn't work."

Patent nonsense. A few years back, I was the largest prescriber of Niaspan in Wisconsin. Although I am embarassed to admit it, I also spoke for the company, educating fellow physicians on the value of niacin for correction of lipid disorders.

Then I shifted to Sloniacin due to cost--it costs 1/20th the cost of prescription Niaspan. I examined the pharmacokinetic data (pattern of release in the body), the published literature (e.g., the famous HATS Trial), and have used Sloniacin over 1000 times in patients. In my experience, there is no difference: no difference in efficacy, no difference in safety, no difference in side-effects. There is a BIG difference in price.

Unfortunately, most pharmacists get their information on niacin from the Niaspan representative.


"You shouldn't be taking vitamin D supplements. I have prescription vitamin D here."

What the pharmacist means is that you should replace your vitamin D3, or cholecalciferol--the form recognized as vitamin D by the human body--with the plant form of vitamin D, vitamin D2 or ergocalciferol.

Since when is a plant form of a hormone (vitamin D is a potent hormone, not a vitamin; it was misnamed) better than the human form?

I've previously talked about this issue in a blog post called Vitamin D for the pharmaceutically challenged.

The notion that D2 is somehow superior to the real thing, D3, is absurd. I use D3 only in my practice and have checked blood levels thousands of times. As long as the D3 comes as a gelcap, drops, or powder in a capsule, it works great, yielding predictable and substantial increases in blood levels of 25-hydroxy vitamin D. If it comes as prescription D2 (or over-the-counter D2), I have seen many failures: no increase in blood levels of vitamin D or meager increases.

Prescription status is no guarantee of effectiveness.


"Why do you need iodine? You already get enough from food."

The NHANES data over the last 25 years argue otherwise: Iodine deficiency is growing, particularly as people are avoiding iodized salt and the iodine content of processed foods is diminishing. The explosion in goiters in my office also suggest this is no longer a settled issue.

On the positive side, it is exceptionally easy to remedy with an inexpensive iodine supplement. That is, until the pharmacist intervenes and injects his bit of nutritional mis-information.


I'm not bashing pharmacists. In fact, Track Your Plaque's own Dr. BG has a pharmacy background, and she is an absolute genius with nutritonal supplements. But she is a rare exception to the rule: Most pharmacists know virtually nothing about nutritional supplements. You might as well ask your hairdresser.

"Healthy" people are the most iodine deficient

Ironically, the healthiest people are the most likely to be deficient in iodine.

Why?

Healthy people tend to:

--Avoid iodized salt because of public health advice to limit sodium
--Use sea salt to obtain minerals like magnesium--but sea salt contains little iodine
--Limit meat--Carnivores obtain more iodine than vegetarians or vegans. In one study, up to 80% of vegans were iodine-deficient (Krajcovicova-Kudlackova M et al 2003).
--Exercise--Substantial amounts of iodine are lost through sweating. In a study of high school soccer players, 38.5% were severely iodine deficient, compared to 2% of sedentary students (Mao IF et al 2001).


That is indeed what I am seeing in my office, as well: The healthiest, most attentive to healthy eating, and most physically active are the ones showing up with small goiters (enlarged thyroid glands) and increased TSH and low free T4 levels.

Why am I checking thyroid and talking about iodine? Because even the smallest degree of thyroid dysfunction can double, triple, or quadruple your risk for cardiovascular events. See the posts Is normal TSH too high? and Thyroid perspective update.

What kind of iodine do you take?

The results of the latest Heart Scan Blog poll are in.

204 respondents answered the question:


Do you take an iodine supplement?

The responses:

Yes, I take Iodoral, Lugol's, or SSKI
26 (12%)

Yes, I take potassium or sodium iodide
19 (9%)

Yes, I take kelp tablets or powder
64 (31%)

No, I rely on generous use of iodized salt
23 (11%)

No, I don't supplement iodine at all
66 (32%)

Isn't iodine something you put on cuts and scratches?
6 (2%)


I am heartened by the number of respondents taking iodine in some form. After all, iodine is an essential trace mineral. Without it and health suffers, often dramatically.

However, I am concerned by the percentage of people who don't supplement iodine at all: 32%. Interestingly, this is approximately the proportion of people who come to my office who also do not supplement iodine who are now showing goiters, or enlarged thyroid glands due to iodine deficiency. Goiters lead to hypothyroidism (low thyroid hormone levels), followed by hyperactive nodules, not to mention undesirable effects like weight gain, fatigue, hair loss, constipation, intolerance to cold, higher LDL cholesterol and triglycerides, and heart disease.

11% of respondents report using lots of iodized salt. This may or may not be sufficient to provide enough iodine to prevent goiter and allow normal thyroid function. The success of this strategy depends to a great extent on how often salt is purchased. Salt that sits on the shelf for more than a month is devoid of iodine, given iodine's volatility.

I am also favorably impressed by the number of people who take "serious" iodine supplements like Lugol's solution, Iodoral, or SSKI. Of course, people who read The Heart Scan Blog tend to be an unusually informed, healthy population. The 12% of people in the poll who take these forms of iodine does clearly not mean that 12% of the general population also takes them. But 12% is more than I would have predicted.

On the Track Your Plaque website, we are awaiting an interview with iodine expert, Dr. Lyn Patrick. I'm hoping for some juicy insights.
All posts by william-davis

High blood pressure vanquished

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado


Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl


I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.


1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.

Restaurant eating: A fructose landmine

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.