Are there any alternatives to niacin?

10. September 2006 William Davis (0)

In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.

Is flaxseed oil a substitute for fish oil?

9. September 2006 William Davis (3)

This question comes up so frequently that it's worth going over.

Flaxseed oil is a wonderful oil rich in linolenic acid, which may provide health benefits all by itself. Some authorities have speculated that the substantial reduction in heart attack seen in the Lyon Heart Study, the study that demonstrated the healthy power of the Mediterranean diet, is due to linolenic acid.

Flaxseed oil is also rich in monounsaturates and low in saturates, both desirable qualities. Of course, I'm talking here about flaxseed oil, to be distinguished from flaxseed , which are the intact seeds. The seeds themselves also contain the same oils, but contain other components, specifically lignan, a plant fiber with suspected health benefits like reduction in cancer risk.

Despite all flaxseed oil's wonderful properties, it is definitely not a substitute for fish oil. Why do we use fish oil for our coronary plaque control program (trying to reduce your heart scan score)? Several reasons. Fish oil:

--Dramatically reduces triglycerides, usually by 50% or more.
--Dramatically reduces specific lipoprotein classes like VLDL
--Dramatatically reduces, often eliminates, abnormal postprandial (after-eating) lipoprotein patterns, like IDL (intermediate-density lipoprotein)
--Has been conclusively shown to reduce risk of heart attack and death from heart attack (GISSI Prevenzione Trial).
--Has been shwon to reduce risk of stroke.
--Modifies blood clotting parameters, particularly a 20% reduction in fibrinogen.

Flaxseed oil, or linolenic acid concentrate for that matter, do not accomplish any of these effects, all crucial if you are to gain control over your coronary plaque.

Flaxseed oil and flaxseed remain wonderful nutritional agents for their own reasons. But they will not substitute for fish oil in your program. Only fish oil--the real thing--does the job.

If you have coronary artery disease . . . do you know why?

9. September 2006 William Davis (0)

This conversation is aimed primarily at non-followers of the Track Your Plaque program, because if you were a follower, you’d already know the answer!

I saw a woman in the hospital today. She’d just survived her second heart attack one week earlier. At 51 years old, she was understandably shaken, perhaps terrified. She felt that her future was uncertain and, in fact, had discussed with her husband what he should do to prepare for a future without her.

One week earlier, she’d received three stents that successfully aborted her heart attack. But, as is always the case, the modest delays of ambulance transport, the emergency room preliminaries, then of mobilizing an available cardiologist and catheterization laboratory team, totaled nearly two hours before her stent procedure. Inevitably, a moderate amount of damage had been done to her heart.

Her first “event” had been very similar: very little warning, then 911 and the flurry of activity. Both times, the cardiologists (two different physicians) complimented the patient on her prompt action. Both also called her heart attacks “close calls”.

She defied the odds with two near-death events. So, when I met her a week after her last heart attack, I asked an obvious question: “Has anyone told you why you’re having these heart attacks?”

She looked completely puzzled at first. She then said, “No, not really. I just assumed it was genetic. My mother went through the same thing when she was my age. But she didn’t get as far as I have, since they didn’t have these procedures back then.”

To me, this seems inexcusable: This woman had experienced two brushes with death and no doctor had established a cause. Could this woman’s belief be true, that it’s just genetic?

While there are, indeed, genetic causes for heart disease, the vast majority of these genetic causes are 1) identifiable, and 2) correctable. Genetic does not necessarily mean hopeless. It just means that the usual equation of heart disease risk management (heart disease = LDL cholesterol = need for Lipitor) has limited value. It would be like giving penicillin to people for any and all infections. It will work occasionally, but it will fail miserably in a great many cases. Treating LDL cholesterol with statin drugs is just like that.

Perhaps this woman has lipoprotein(a), a serious genetic trait that predicts heart disease at a young age and is largely unaffected by statin drugs. Or, she may have a severe excess of small LDL, only partially suppressed by statins. If she has the combined pattern of lipoprotein(a) and small LDL, that means she has two statin-unresponsive and significant genetic traits. But they respond to niacin, specific nutritional strategies, and several other agents.

The message: If you have coronary disease, you need to insist on knowing why. “It’s genetic” is not an acceptable answer. “There’s no proof of any heart disease causes beyond cholesterol” is also nonsense. “Everyone gets heart disease, or “hardening of the arteries”, eventually. You just got it a little before everyone else” is also patently ridiculous.

Identifying the causes of your coronary disease (or coronary plaque if you’ve had a CT heart scan) is the first step in developing a program of treatment that provides you with control over this disease.

Have you tried inulin yet?

8. September 2006 William Davis (0)

If you haven't yet tried it to facilitate weight loss, it's really worth giving the new inulin-containing product, Fiber Choice "Weight Management", a try.

Recall (from a prior Heart Scan Blog) that inulin is a vegetable-based fiber found in celery, green peppers, etc. that, when exposed to water, expands to many times original volume. This simple phenomenon yields satiety--a feeling of fullness.

The manufacturer of the product has also added green tea, which has been shown in two small clinical studies to enhance weight loss, though by a different route.

We've been advising patients to chew two of the strawberry flavored tablets one hour before every meal (or with breakfast if you eat immediately in the morning). You'll be satisfied with less food and you'll experience less intense food cravings.

Though no one so far has achieved a huge drop in weight, it does seem to enhance a slow, gradual weight loss larger than achieved by diet and exercise alone. And it's very safe and inexpensive. If you give it a try to help you lose weight, let us know what kind of results you've obtained.

Fish oil update on Life Extension

6. September 2006 William Davis (1)

An article of mine came out in Life Extension Magazine and is available on the online version at:

http://www.lef.org/magazine/mag2006/sep2006_report_omega1_01.htm

This is an update on the heart health applications of fish oil.

Or, go to to www.lef.org and put fish oil into your on-site search and you'll come back to it in future.

Of course, it comes with Life Extension's promotion of its supplements.

Although it's not yet available online, the hard copy version of an article I wrote on homocysteine is available in the October, 2006 Life Extension Magazine. If you're not a member of their program, they'll send you a free copy just for signing up for it without obligation. Go to the home page of www.lef.org to do so. Or, Life Extension is available at newstands if you're in a rush or don't want to sign up for a free copy.

More on Vitamin D

6. September 2006 William Davis (0)

If you haven't done so already, you should subscribe to Dr. John Cannell's free newsletter on vitamin D issues. His newest issue is available at:

http://www.vitamindcouncil.com/newsletter/2006-aug.shtml

A sign-up to subscribe is available on the same page.

I continue to be shocked and amazed at the prevalence and magnitude of vitamin D deficiency in the people I see every day. It's been a beautiful summer with very little rain. Most days have been in the 70-80 degree range--very comfortable to be outdoors in the sun and getting skin expoxure to activate vitamin D in the skin.

Yet, in the vast majority of people I see, summer blood levels of vitamin D are virtually indistinguishable from winter levels. Both hover around the 30 ng/ml range. Summer levels in Wisconsin people seem to be no more than 10 ng/ml higher than winter levels. This remains true even in people who spend a lot of their day outdoors gardening, walking, etc. wearing shorts and a short-sleeved shirt, i.e. with plenty of skin surface area exposed.

I'm at a loss to explain precisely why. Yes, it is Wisconsin. But a direct sun overhead, 75 degree day should be providing plenty of sun. My suspicious is that a combination of factors are at work: people are not spending as much time outdoors as they claim; they often seek shade; use sunscreen; and they're overweight. (Excess weight decreases vitamin D blood levels dramatically, yet another reason not to get fat!)

Read more about vitamin D by checking out Dr. Cannell's insightful comments on the unfolding vitamin D story. He holds nothing back.

Why not just get "perfect" lipids and call it a day?

5. September 2006 William Davis (0)

What if you achieved the Track Your Plaque lipid targets: LDL cholesterol 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl?

After all, these are pretty stringent standards. Compared to national guidelines (the ATP-III Guidelines of the National Cholesterol Educational Panel), the Track Your Plaque 60-60-60 goals are laughably ambitious. There's a lot of wisdom hidden in those numbers. The triglyceride level of 60, for instance, is a level at which triglycerides become essentially unavailable for formation of triglyceride-containing lipoprotein particles such as small LDL and VLDL.

If you get to the 60-60-60 target, isn't that good enough? What if you just held your values there and went about your business? Will coronary plaque stop growing and will your CT heart scan score stop increasing?

Sometimes it will. But, unfortunately, many times it will not. The experience generated through clinical trials bear this out. Studies like the St. Francis Heart Study and the BELLES Trial both showed that just reducing LDL cholesterol is insufficient to stop plaque growth. Beyond the Track Your Plaque experience, there's no clinical trial experience that shows whether the 60-60-60 approach does any better.

In our experience, achieving 60-60-60 is indeed better than just reducing LDL. That makes sense. Just raising HDL from the average of 42 mg/dl for a male, 52 mg/dl for a woman adds advantage. Compound this with triglyceride reduction from the plaque-creating equation, and you've doubled success.

But there's even more. What if you had hidden patterns not revealed by conventional lipids? How about lipoprotein(a)? Small LDL? Postprandial (after-eating) abnormalities? Hypertensive effects (more common than you think)!

In 2006, stopping the increase in your heart scan score is, for most of us, not just a matter of taking Lipitor or its equivalent and sitting back. For nearly all of us, stopping the progression of your score is a multi-faceted effort.

Hospitals: Then and Now

2. September 2006 William Davis (0)

It's 1920. The hospital in your city is a facility run by nuns or the church. It's a place for the very ill, often without hope of meaningful treatment, but nonetheless a place where surgeries take place, babies are born, the injured and chronically ill can find care. No one has health insurance and there's no Medicare. Everyone pays what they can. The hospital is accustomed to doling out plenty of care without compensation. For that reason, they welcome donations and sometimes will build new additions or other facilities in honor of a major donor.

Volunteeers are common, since the wards are understaffed and generally suffering from a shortage of trained nurses and personnel associated with the church. Drugs, such as they are, are often prepared from basic ingredients in the hospital pharmacy. Product representatives hawking medicines and devices are virtually unheard of.

Though their therapeutic tools are limited, the physicians are a proud group, dedicating their careers to healing. The majority of the medical staff volunteer large portions of their time to care for the poor who come to the hospital with very advanced stages of disease: metastatic tumors, advanced heart failure, debilitating strokes, overwhelming septicemia, etc.

Hospitals are usually governed by a board of clergy and physicians who make decisions on how to apply their limited resources and continually seek charitable donations.

Fast forward to present day: Hospitals are high-tech, professional facilities with lots of skilled people, complicated equipment,and capable of complex procedures. While they still house people with advanced illnesses, the floors are also filled with people with much earlier phases of disease. In general, they do a good job, with quality issues scrutinized by a number of official agencies to police practices, incidence of hospital-related infections, medication errors, care protocols, etc.

The hospital of 2006 is a more more effective place than the hospital of 1920. But its aims and operations are different, also. Though some churches are still involved in hospitals, more and more are owned by publicly-traded companies that answer to shareholders--shareholders who want share value to increase. Though donations are still sought, much of the revenues are obtained by concentrating on profitable, large-ticket procedures. More procedures are often generated by advertising.

Because they operate to generate profits, several hospitals in a single city or region compete with one another. The 21st century has therefore witnessed the phenomenon of hospital-owned physicians: more and more practicing physicians are employees of their hospital. That way, the physician brings all his patients and procedures to his hospital, not to a competitor. The top of the funnel is the primary care physician, who tends to see all disease when it first occurs. The primary care physician then sends the patient to the specialist, who is obliged (by contract) to perform his/her procedure in the hsopital paying their salary.

Representatives from companies manufacturing and selling expensive hospital equipment and drugs are everywhere, falling over themselves to gain attention of the physicians using their equipment and the hospital buyers who make purchasing decisions. Millions of dollars can be transacted with just one sale.

The number of volunteers has dwindled. The poor and uninsured are commonly diverted elsewhere, often to a government-funded, and often second-rate, institution. Hospitals measure success by comparing annual revenues and numbers of major procedures.

The hospital of 2006 is a vastly different place than 1920. If you're expecting charitable treatment, compassion, and selfless care, you're in the wrong century. In 2006, the hospital is a business. You don't expect charitable treatment at Wal-Mart or from your car dealer. Don't expect it from your hospital. They are businesses and you are a customer. Recognize this fact, lose the nostalgia for the hospitals of yesterday, and a lot more will become clear to you.

The dreaded small LDL particle

1. September 2006 William Davis (0)

Brian is a 59-year old landscape architect whose starting CT heart scan score was 276.

Brian's food choices at the start were deplorable: a pound of sausage per week, sometimes more; butter on anything and everything; up to two pounds of cheese per week; hot dogs; etc. His lipoproteins were accordingly just as miserable: low HDL, high triglycerides, excessive (postprandial, or after-eating) IDL. Small LDL was a particularly stand-out pattern, with 95% of all LDL particles in the small category.

Brian made a dramatic turnaround in lifestyle and corrected all of his patterns--except for small LDL. After one year, small LDL still occupied 95% of all LDL particles, even though the quantity of LDL had been reduced. In order to help convince Brian that correction of his small LDL was going to be necessary to achieve control oover coronary plaque, I suggested that he undergo another heart scan. His score: 435, or a 57% increase.

Each day that passes, I gain more and more respect for small LDL as a cause for coronary plaque growth. Conventional thought among lipid experts is that small LDL should no longer be a factor if total LDL (e.g., LDL particle number) is reduced. But our experience suggests otherwise: when small LDL persists, we tend to see continued, sometimes frightening, plaque growth.

I therefore asked Brian to intensify his efforts: additional weight loss off his somewhat prominent abdomen (since visceral fat increases small LDL), further reduce wheat products and processed carbohydrates, increase niacin (to 1500 mg per day), and use more raw almonds and oat bran.

Don't let small LDL get the best of you. It is a nasty, sometimes persistent abnormality that has impressive effects on plaque growth.

Winning Through Intimidation

31. August 2006 William Davis (0)

Do you remember the book, Winning Through Intimidation by author Robert J. Ringer?

In his 1984 bestseller, author Ringer details how to succeed in business by overwhelming clients and competition by appearing hugely successful and powerful. Rather than a business card, he'd hand out an elegant book to represent himself. He'd show up in a limousine to a meeting, even when he could barely afford it. He used these tactics, even when he was a small-fry, in commercial real estate and built a successful business following such techniques.

This reminds me a lot of what happens in conventional medical practice: The large and successful hospitals, filled with trained staff and technology, exude legitimacy and success. How can they possibly be wrong? Such overwhelming know-how and multiple levels of expertise mustbe right!

Let's be grateful that we do have access to such high-tech, capable care. Unfortunately, just as Mr. Ringer used deceptive practices to appear something he wasn't, this is also true in hospitals. Not all physicians have your best interests in mind. Their principal concern is how profitable your care can be for them--can you be persuaded to have your stent, bypass, etc.. After all, look around you: Aren't all this equipment and personnel impressive? Aren't you intimidated?

The patient that most recently drove home this issue for me recently was a smart and capable executive who came in for consultation. He had been told by his internist that a surgery (to replace his aorta, a HUGE procedure) was probably necessary. In my view, it was not--his process was simply not that far progressed. The risks for danger over the next several years was virtually nil. Unfortunately, this man, now confused and worried, sought an opinion from the chief of thoracic surgery (in the usual white coat and with professorial demeanor, I'm sure) in a major metropolitan hospital (in Chicago), who promptly rushed him off to the operating room.

The pathology report, cleverly not mentioned in any other of the hospital documentation, showed what I had suspected: this man had mild disease that wasn't even close to requiring surgery. But, with all that technology, $100,000 or so of costs, chief of surgery who looked the part, etc.--they must be right!

Robert Ringer's concepts only ring too true for hospitals and some of the unscrupulous physicians in practice. Don't allow yourself to be intimidated.

All posts by william-davis

Take a niacin "vacation"

20. November 2006 William Davis (2)

I've been seeing a curious niacin phenomenon that has not, to my knowledge, been reported anywhere in the medical literature.

People with lipoprotein(a), or Lp(a), are best treated with niacin, particularly given the relative lack of other effective therapies. I now have seen approximately 10 people with great initial responses to niacin, only to observe Lp(a) levels slowly drift back up to the starting level over a period of 2-3 years.

In other words, if starting Lp(a) is 200 nmol/l (approximately 80 mg/dl), drops to 70 nmol/l on niacin. Then, over 2-3 years of treatment, it drifts back to 200 nmol/l. Very frustrating.

Somehow, your body's Lp(a) manufacturing mechanism circumvents the niacin, sort of like antibiotic resistance (without the bacteria, of course).

My response to this, though untested, is to have people take an occasional "niacin vacation". I don't mean take a trip to the Bahamas while on niacin. I mean take 2 weeks off from niacin every three months or so. My hope is that the occasional vacation from niacin will allow the body to continue to respond and suppress "resistance". When resuming niacin, you may have to escalate the dose gradually to avoid re-provoking the "flush".

The same "resistance" seems to develop to testosterone in males: an initial drop followed by a gradual increase. Curiously, I've not seen this in females with estrogens, which seems to generate a durable Lp(a) suppressing effect. For this reason, an occasional testosterone "vacation" might also be considered.

So far, I've advised several people to try this. The long-term success or failure, however, is uncertain. I know of no other solutions, however.

If you have Lp(a) and are on long-term niacin, you should consider talking about this issue with your physician. Like many aspects of Lp(a), while fascinating in its complexity, much remains uncertain. Stay tuned.

When LDL is more than meets the eye

18. November 2006 William Davis (0)

Jerry wanted to know what to do with his LDL cholesterol of 112 mg/dl. "My doctor said that it's not high but it could be better."

So I asked him what the other numbers on his lipid panel showed. He pulled out the results:

LDL cholesterol 112 mg/dl

HDL 32 mg/dl

Triglycerides 159 mg/dl

I pointed out to Jerry that, given the low HDL and high triglycerides, his calculated LDL of 112 was likely inaccurate. In fact, if measured, LDL was probably more like 140-180 mg/dl. LDL particles were also virtually guaranteed to be small, since low HDL and small LDL usually go hand-in-hand (though small LDL can still occur with a good HDL).

So Jerry's LDL is really much higher than it appears. To prove it, Jerry will require an additional test, preferably one in which LDL is measured, such as LDL particle number (NMR), apoprotein B, or "direct" LDL.

It's really quite simple. Jerry likely has a high number of LDL particles that are too small. This pattern confers a three- to six-fold increased risk for heart disease.

Treatment requires more than just reducing LDL. Small LDL--an important component of this pattern, responds, for instance, to a reduction in processed carbohydrates like wheat products (breads, breakfast cereals, pretzels, etc.), NOT to a low-fat diet. Weight loss to ideal weight, especially loss of abdominal fat, will yield huge improvements in these numbers. Niacin may be a necessary component of Jerry's treatment program, since it increases LDL size and raises HDL.

For more discussion on measures superior to LDL cholesterol, see my upcoming editorial, Let Dr. Friedewald Lie in Peace (an expansion of a previous Heart Scan Blog). It will be posted on the Cardiologist on Call column on the Track Your Plaque website within the next week.)

Oil-based vitamin D

14. November 2006 William Davis (2)

As time passes, I gain greater and greater respect for the power of restoring vitamin D blood levels to normal, i.e. 50-70 ng/ml. Just yesterday, I saw several people with blood levels of <10 ng/ml--severe deficiency.

Vitamin D deficiency this severe poses long-term risk for osteoporosis, arthritis, colon cancer, prostate cancer, inflammatory diseases, diabetes, and heart disease. Vitamin D appears to make coronary plaque reversal--reduction of your heart scan score--easier and faster.

But it is important that you take the right kind of vitamin D. Several of the people I saw yesterday with vitamin D levels of somebody living in total darkness were taking vitamin D, but they were taking tablets. Tablets are the wrong form. Powder-based tablets, in my experience, yield little or no rise in blood levels. Some preparations generate a small rise but the dose required is huge.

If you're going to take vitamin D, take a preparation that yields genuine and substantial rises in blood levels. This requires an oil-based capsule. I commonly see blood levels of 25-OH-vitamin D3 rise from, say, 10 ng/dl to 60 ng/ml when oil-based capsules are taken.

The most common dose I prescribe to patients is 2000 units per day to females, 3000-4000 units per day to males in non-sun exposed months. Ideally, your dose is adjusted to blood levels.

The Vitamin Shoppe preparation pictured here is one I've used successfully and generates bona fide rises in blood levels. And it costs around $5. Just be sure the preparation you buy is oil-based.

For rapid success, try the "fast" track

14. November 2006 William Davis (1)

Have you tried fasting?

Before your eyes glaze over, let me tell you what I mean. I don't mean a water-only fast for two weeks while you drool over all the temptations around you and you feel sorry for yourself.

I also don't mean the juice fasts that some people use that turn into fruit juice fasts of pure sugar.

Here's another way to do it. Usually, 48 hours of doing this will yield several benefits:

--Weight loss of 1 lb. You will likely experience an even greater weight loss of 2-4 lbs, but much of this will be water loss.

--If you're like me and share a heightened sensitivity to sugars and carbohydrates (like wheat), you may find out just how awful you feel when you eat certain foods. Many people tell me they feel absolutely wonderful when they fast--clearer thinking, increased energy, improved mood. Not the constant gnawing urge to eat they expected.

--After your fast is over, you look back and realize just what large portions of food you were eating. You'll be content with smaller quantities--and enjoy it more.

The "fast" I've used successfully includes two foods:

1) Vegetable juices--that you either juice yourself or purchase. V8 or its equivalent works pretty well. Though purchased V8 is not the best, it's better than nothing and does work reasonably well. If you juice your own vegetable juices, watch out for the diarrhea if you're unaccustomed to vegetable juices. Four 8 oz glasses per day works well.

2) Soy milk--for a source of protein and modest quantity of sugar and fat. I like the Light Silk Soymilk (Vanilla) which contains 80 calories, 2 g fat (0.5 g monounsaturated), 7 g sugar, 6 g protein per 8 oz glass. Four 8 oz glasses of soymilk also work well.

In my neighborhood, 8th Continent is another good choice.

Sip both of these throughout the day. Of course, drink water in unrestricted amounts.

What can you expect in your coronary plaque control/heart scan score reversal program? When the fast is over, a rise in HDL, reduction in small LDL, reduction in triglycerides, reduction in blood sugar and insulin, and a smaller tummy. This strategy can be useful to kick-start weight loss efforts or as a periodic way to maintain control over weight and lipid/lipoprotein patterns.

Nutritional Composition Silk Soymilk--Vanilla

Nutrition Facts
Serving Size 1 cup (240mL)
Servings per container 8 H/G OR 4 QT

Amount per Serving

Calories 70
Calories from Fat 20

% Daily Value
Total Fat 2g 3%
Saturated Fat 0g 0%
Trans Fat 0g
Polyunsaturated Fat 1g
Monounsaturated Fat 0.5g

Cholesterol 0mg 0%
Sodium 120mg 5%
Potassium 300mg 8%
Total Carbohydrates 8g 3%
Dietary Fiber 1g 4%
Sugars 6g
Protein 6g
Vitamin A 10%
Vitamin C 0%
Calcium 30%
Iron 6%
Vitamin D 30%
Riboflavin 30%
Folate 6%
Vitamin B12 50%
Magnesium 10%
Zinc 4%
Selenium 8%

No flush = No effect

13. November 2006 William Davis (3)

"Inositol Hexanicotinate is the true 'flushless niacin.' Unlike 'sustained-release' niacin, which is just regular niacin in a pill which dissolves more slowly, Inositol Hexanicotinate is a niacin complex, formed with the B-vitamin-like inositol. When you take an IHN supplement, the central inositol ring gradually releases niacin molecules, one at a time delivering true niacin. This, like “sustained-release” niacin, allows you to take niacin at clinically-proven doses without going crazy with the itch."

That above bit of nonsense adorns one manufacturers sales pitch for its no-flush niacin. No-flush niacin is one of the biggest scams in the health food store.

Ordinarily, I love health food stores. There's lots of fun and interesting things available that pack real power for your health program. Unfortunately, there's also outright nonsense. No-flush niacin is absolute nonsennse.

No-flush niacin is inositol hexaniacinate, or an inositol molecule complexed with 6 niacin molecules. So it really does contain niacin. However, although it works in rats, it exerts no known effect in humans.

Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

The lack of any observable effect and no studies whatsoever showing a positive effect (there is one study demonstrating no effect), manufacturers continue to manufacture it and health food stores continue to push it as an alternative to niacin that causes the flush. It's quite expensive, commonly costing $30-$50 for 100 tablets.

Don't fall for this gimmick. Niacin is among the most helpful of treatments for gaining control over coronary plaque. It raises HDL, corrects small LDL, reduces triglycerides (along with its friend, fish oil, of course), reduces lipoprotein(a), and dramatically contributes to reduced heart attack risk. No-flush niacin does none of this. Track Your Plaque Members: For a thorough discussion of niacin--how to use it, what preparations work and which do not, read Niacin: Ins and outs, ups and downs on the www.cureality.com website.

"Black holes" on heart scan

11. November 2006 William Davis (1)

Lots of smokers, especially younger smokers, rationalize their habit by telling themselves that they'll stop if and when any hint of adverse health effects develop.

The problem is that, even in the first decade of smoking, dramatic and profound effects can develop--but you won't know it.

One of the most graphic examples of this I see every day in people who have heart scans. While CT heart scans are, of course, for identification of coronary plaque/coronary disease, they're also great for visualizing the lungs.

This man is a light smoker. The lungs are the black tissues (that's normal) on either side of the (white) heart in the center. Now, note the holes in the lung tissue. That's what they literally are: holes left by the destrucive, tissue-eating effects of cigarette smoking.

How common are the holes (or emphysematous "blebs", as they're called in medical lingo)? Very common. You'll even see them in 30-somethings who've smoked only a few years.

These are holes that have nothing in them. The lung tissue that was destroyed to create the hole will never grow back, even when smoking stops. The holes in this example are actually small to average in size. I've seen much bigger. And this only represents the early stages of lung tissue destruction. A long-time heavy smoker shows all other sorts of abnormalities.

Whenever I show these "black holes" to people who smoke, they are horrified and I've actually gotten many people to quit. Take the opportunity to quit as soon as you can if you smoke.

Small LDL--a persistent bugger

10. November 2006 William Davis (1)

Sometimes, small LDL is easy to get rid of. Take niacin, for instance, and it can simply disappear from your body.

But other times, it can be aggravatingly persistent. Several times every day, in fact, I need to run through the checklist of strategies to reduce small LDL with patients.

How important is small LDL? In my experience, it is among the most potent causes behind coronary plaque known. It's a big part of the explanation why some people at an LDL of cholesterol of X mg/dl will have heart disease, while others with the same X mg/dl of LDL will not. When present, small LDL particles are much more likely to trigger atherosclerotic plaque formation. Small LDL particles magnify Lp(a)'s ill-effects tremendously. The data vary but small LDL probably increases heart attack risk at least three-fold.

Here's a checklist of strategies that I advise patients to consider to minimize the small LDL pattern:

--Lose weight to ideal weight--This is very important and effective.

--Fish oil--A relatively small effect unless triglycerides are high to begin with.

--Reduction of wheat products--This can provide a BIG effect. More precisely, a reduction in high-glycemic index foods is effective. But the biggest day-to-day high-glycemic food culprits are wheat products like breads, pasta, crackers, chips, pretzels, and breakfast cereals. "You mean whole wheat bread makes small LDL?!" Yup.

--Reduction of sweets--For the same reasons as reducing wheat products.

--Add raw almonds and walnuts--1/4 to 1/2 cup per day.

--Replace wheat products with OAT products, especially oat bran. This does NOT mean oat-containing breakfast cereals with added sugar and wheat, e.g., Honey Nut Cheerios, Cracklin' Oat Bran Cereal, etc. You might as well eat candy. Buy oat bran as plain oat bran--nothing added. Use it as a hot cereal or added to yogurt, "breading" for chicken, etc.

--Vitamin D--A variable effect, likely resulting from its beneficial effects on "insulin resistance".

--Exercise

--Niacin--Very effective but not always enough.

Among the choices, my favorites are weight loss, niacin, and reduction of wheat products. Those will give you the biggest bang for your buck.

Red badge of courage

8. November 2006 William Davis (0)

A group of 60- and 70-somethings were standing in the anteroom to the cardiac rehabilitation center. All (males) had their T-shirts pulled up, comparing their coronary bypass scars.

It reminds me of war veterans comparing their war wounds. The scars of suffering, of having "conquered" and won a war with a common enemy, a badge of courage.

This is part of the broad social acceptance of bypass surgery and other major procedures for heart disease. Hospitals support it. They do it for the psychological support for patients enduring a difficult process. Often, talking about a shared experience can be a helpful purge for the fears and frustrations of a traumatic event.

Curious thing, though. I've actually had people request bypass surgery simply because all their friends have had one. No kidding. "I just figure my time is coming. I might as well get it over with."

Get the picture? We've had a battle with heart disease and the hospitals have won. The enormous success of hospitals over the last 20 years is not because of delivering babies, it's not from psychiatric hospitalization, it's not from cancer treatment. It's from heart disease. The largest floors in the hospital are usually the cardiac floors. The bulk of revenues and profit are from heart disease.

If I manufacture widgets and each widget I sell makes me scads of money, guess what? I want to sell more and more widgets. I'll persuade people they need my widgets even if they don't. Perhaps I'll even persuade them that buying one is a noble cause. Maybe I'll subtly suggest that I am a charitable operation and I only sell my products for the public good. I could even name my company after a saint. Personal profit--absolutely not!

Ignore the hype. See hospitals and their "products" for what they are: A necessary service--some of the time; profitable products that they hope to sell to more and more people most of the time.

"We don't believe in heart scans"

7. November 2006 William Davis (0)

Tim's CT heart scan score was an earth-shattering 3,447, clearly in the upper stratosphere of percentile rank. Risk of heart attack: 25% per year. At age 58, it was a wonder that nothing had happened yet.

Tim went to the Cleveland Clinic for an opinion, long a powerful bastion of heart procedures. The consulting cardiologist told Tim, "We don't believe in heart scans. They're wrong too often."

An opinion from a widely-respected cardiovascular center. If they don't "believe" in heart scans, does that mean they "believe" in stents and bypass surgery? Does it mean that the thousands of research studies that have now been published on the value of heart scanning are pure fiction? Is there a choice to believe or not believe?

I continue to be shocked at the extraordinary ignorance on the topic of heart scanning among my colleagues. The number one killer of Americans and you still rely on stress tests?

Why this perception that heart scans are "wrong too often"? What this cardiologist means, I believe, is that when people are taken to the cath lab for catheterization, a substantial number of those with positive heart scan scores don't have "blockage". But I could have told him that even before the heart catheterization.

There is an expected and well-documented likelihood of finding significant "blockage" based on your heart scan score. At Tim's scary score of 3,447, what is the likelihood of "blockage" of 50% or more? It's around 40-50%. That means that half the people at this score will have a blockage sufficient to justify inserting stents or undergoing bypass surgery, half will not. There will indeed be many plaques, but none severe enough to block flow.

Does that make the heart scan wrong? I don't think it does. Just because you don't need a major procedure to "fix" blockages does not mean that no heart disease is present. Without preventive efforts, Tim's heart attack risk remains an alarming 25% per year--whether or not he gets stents or bypass. The only treatments that substantially reduce this risk (in an asymptomatic person) are preventive efforts, not procedures.

Yet cardiologists like the one Tim consulted at the Cleveland Clinic regard heart scans as something "he doesn't believe in". I would suggest a return to the textbooks and published literature and re-thinking how heart disease should be managed.

Heart scans should provide an opportunity for prevention, not an opportunity for profit.

More on the “Rule of 60”

6. November 2006 William Davis (0)

Despite its apparent simplicity, there’s a lot of thought and wisdom in the Rule of 60.

What if you achieve only a single value in the Track Your Plaque “Rule of 60”? What if, for instance, you got LDL down to 60 mg/dl, but ignored the fact that your HDL was 41 mg/dl and triglycerides were up to 145 mg/dl? Can you still do pretty well?

Probably not. In fact, this specific combination of low HDL and high triglycerides tells me several things:

1) LDL is really much higher than suggested by the 60 mg/dl, which is a calculated value, often much higher. Recall that calculated LDL is prone to immense inaccuracy. When measured, the LDL is commonly somewhere between 120 and 160 mg/dl. However, when you raise HDL to 60 and reduce triglycerides to 60, much of the inaccuracy is removed, i.e., calculated LDL becomes more accurate. LDL can be measured as LDL particle number (NMR), apoprotein B, or direct LDL.

2) LDL particles are small. This is yet another reason why the weight-based LDL measures can be inaccurate. Imagine you have two identical glass jars full of marbles. One jar has small marbles, the other has large marbles, but both jars have the same weight in marbles. Which jar has more marbles? The one with small marbles, of course. The same phenomenon occurs with LDL particles: at the same weight, you can have different numbers of LDL particles. It’s the number of particles that better determine risk for heart disease, not the weight.

3) Triglycerides of 145 mg/dl is actually below the target advised by the National Cholesterol Education Panel Adult Treatment Panel-III guidelines, i.e., you’re okay by conventional standard. But look beneath the surface, and you’ll find that triglycerides at 145 mg/dl are associated with flagrant excesses of VLDL lipoprotein particles and a greater likelihood of a postprandial (after-eating) disorder (increased IDL or postprandial triglycerides), both of which add to coronary plaque.

4) This pattern is also commonly associated with higher blood sugar, higher blood pressure, increased inflammation (e.g., C-reactive protein), increased fibrinogen—all the facets of the metabolic syndrome, or pre-diabetes.

In fact, some of the most aggressive plaque growth—increasing heart scan scores—will occur with this specific pattern. So just achieving one facet of the Track Your Plaque Rule of 60 does not suffice. It’s the whole package that really stacks the odds in your favor of stopping or dropping your heart scan score.

You just THINK you're low-carb

27. febrero 2010 William Davis (72)

Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people.

I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.

Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:

Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people.

Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.)

Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher.

Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars.

A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits.

Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food.

The LDL-Fructose Disconnect

26. febrero 2010 William Davis (8)

I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.

This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.

32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:

Increased LDL cholesterol (calculated) by 7.6%

Increased Apoprotein B (a measure of the number of LDL particles) by 24%

Increased small dense LDL by 41%

Increased oxidized LDL by 12.6%

In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.)

This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry.

I told you bread was bad

26. febrero 2010 William Davis (10)

"I dream about bread"

25. febrero 2010 William Davis (14)

Marion sat in my office, sobbing.

It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips.

"I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"

Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)

This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread.

Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:

14 lbs weight loss in 14 days

Increased mental clarity, reduced moodiness, deeper sleep

70% reductions in small LDL

More than 300 mg/dl reductions in triglycerides

Relief from chronic scalp rash

I could go on.

All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains."

70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet.

You won't know until you try.

Prototypical Lipoprotein(a)

25. febrero 2010 William Davis (23)

Here's the prototypical male with lipoprotein(a):

Several features stand out in the majority of men with lipoprotein(a), Lp(a):

Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight.

Intelligent--Above average to way above average intelligence is the rule.

Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a).

Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Are rabid fans of Star Trek.

Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a).

Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise.

Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.

Gastric emptying: When slower is better

20. febrero 2010 William Davis (18)

When it comes to the Internet and Nascar, speed is good: The faster the better.

But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better.

Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss.

Strategies that can slow gastric emptying include:

--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%.

--Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl.

--Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties.

--Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates.

Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse.

However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk.

Genetic vs. lifestyle small LDL

19. febrero 2010 William Davis (59)

Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)

Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)

Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L (193/1810 = 10.6% of total)

Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L (729/1113 = 65.4% of total)

Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Carbohydrate sins of the past

17. febrero 2010 William Davis (15)

Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Saturated fat and large LDL

16. febrero 2010 William Davis (44)

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles

For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Is glycemic index irrelevant?

14. febrero 2010 William Davis (20)

University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.

All posts by william-davis

China fiction?

10. July 2010 William Davis (39)

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

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

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

Her comments on the relationship of wheat to heart disease:

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

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

Carbohydrate-LDL double whammy

9. July 2010 William Davis (14)

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

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

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

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

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

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

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

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

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

To lose weight, prick your finger

8. July 2010 William Davis (45)

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

So how can you stop triggering insulin?

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

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

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

To do this, you will need:

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

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

Iodine update

2. July 2010 William Davis (30)

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

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

Among the phenomena I've observed:

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

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

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

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

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

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

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

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

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

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

1. July 2010 William Davis (26)

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

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

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

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

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

Easy: Because the treatments are nutritional and inexpensive.

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

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

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

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

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

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

Now you know better.

How to have a heart attack in 10 easy steps

29. June 2010 William Davis (48)

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

1) Follow a low-fat diet.

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

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

4) Use cholesterol-reducing plant sterols.

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

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

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

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

9) Neglect sun exposure and vitamin D restoration.

10) Limit your salt intake while not supplementing iodine.

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

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

Kick inflammation in the butt

25. June 2010 William Davis (0)

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

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

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

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

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

Why not just correct the underlying causes?

Life without Lipitor

25. June 2010 William Davis (17)

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

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

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

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

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

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

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

In search of wheat: Emmer

23. June 2010 William Davis (13)

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

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

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

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

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

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

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

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

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

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

In search of wheat: Another einkorn experience

23. June 2010 William Davis (6)

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

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

Here's Lisa's experience:

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

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

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

10:05 am
BG 99

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

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

11:05 am
1hr PP 120

11:35 am
90 mins PP [postprandial] 113

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

12:50 pm
BG 100

Before dinner 5:10 pm
BG 88

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

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

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

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

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

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

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

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