Conventional therapy vs. alternative therapy

11. March 2008 William Davis (5)
Rose is a 75-year old woman, mother of four, grandmother of many more.

Rose's story started after a heart attack 18 months ago that resulted in two stents. She was advised to follow an American Heart Association diet and take Lipitor. However, some months later, after her fourth stent, she became disilluioned in the conventional approach to heart disease and sought alternative therapies to help reduce or reverse her heart disease.

She found an alternative health practitioner who advised chelation, antioxidant vitamins for "excessive oxidation," and several homeopathic preparations.

Nothing was said about diet or exercise. Nothing was said about the baked flour products and pastries that occupied at least two meals every day. Nothing was said about the candies she indulged in several times per day, nor the soft drinks. Nothing was said about the wildly fluctuating blood sugars, poorly controlled by an oral diabetes agent. Thirty pounds of weight gain over the past 5 years with no exercise or physical activity? No comment here, too.

In short, Rose was the "graduate" of the conventional approach, as typically offered nationwide thousands of times a week. She was also the recipient of the insight of at least one alternative health practitioner, eager to reject conventional notions of how to achieve heart health.

So I then met her. She was experiencing chest pains every day, several times per day. Blood pressure over 200. At 5 ft, 3 inches, weight: 186 lbs.

Initial laboratory results:

HDL cholesterol 42 mg/dl
LDL 132 mg/dl
Triglycerides 263 mg/dl
Blood sugar 173 mg/dl


You can fill in the rest. In short, Rose was a disaster. Despite the attentions of several professionals from both the conventional as well as alternative camps, she was careening rapidly towards failure. She'd been given various crutches, Band-Aids, and salves, none of which resulted in any possibility of long-term relief from her aggressive disease.

My point: As I've said previously, all we want is truth. We want effective, rational approaches that yield real benefit. A stent? All that provides is temporary restoration of blood flow. Statin agents? They do indeed reduce LDL cholesterol. But what if Rose has 8, 9, or 10 other causes of heart disease unaffected by the statin drug? It will do little or nothing.

Nobody had addressed many of the root causes of Rose's disease: insulin resistance, high triglycerides, inactivity, obesity, hypertension (and identifying the reasons why her blood pressure was so high), vitamin D deficiency (virtually guarantted to be severe), junk foods including the ones known as "whole grains."

My message: Success in heart disease, as well as all aspects of health for that matter, doesn't necessarily have to come from an "alternative" approach, nor a "conventional" approach. It comes from applying what is truly effective, regardless of what label someone applied to it.

I would no sooner trust my health and life to an alternative health practitioner hawking unusual herbs and remedies than I would submit to a heart catheterization, three stents, followed by a statin drug. There's small benefit in both approaches, but none are the best. You've got to look elsewhere for that.


Copyright 2008 William Davis, MD

The JELIS Trial

9. March 2008 William Davis (5)
The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about.

This enormous trial followed a simple design:

Japanese men, between 40-75 years, and Japanese postmenopausal women aged <75 years with total cholesterol 250 mg/dl or greater were enrolled. A total of 18,645 subjects (mean age, 61 years; 31% male) participated: 36% had hypertension, 15% had diabetes, and 20% had coronary disease (history of heart attack or heart procedure). Average starting total cholesterol 275 mg/dl; LDL 180 mg/dl. All participants were treated with pravastatin 10 mg/day or simvastatin 5 mg/day; approximately half also received the omega-3, EPA, 1800 mg/day, in addition to one of the statin drugs.

Treatment resulted in an average LDL reduction of 26% in all participants; the group taking EPA experienced an additional 10% reduction in triglycerides. All major cardiovascular events were tracked and tabulated, including sudden cardiac death, fatal or nonfatal myocardial infarction (MI), unstable angina pectoris, coronary artery bypass surgery, and coronary angioplasty.

After nearly five years, 3.5% of statin-only participants experienced an event; 2.8% of statin + EPA experienced an event. The (often misleading and frequently abused value) "relative reduction" was therefore 19%.

There are several features that make the JELIS trial interesting:

--There were an unusually low number of cardiovascular events in the entire group, lower than nearly all American and European trials of similar design. This likely points to the greater burden of atherosclerotic heart disease in the U.S. compared to Japan. Rates in comparable U.S.-based trials usually range from 6-14%, sometimes more.

--Both the participants without identified heart disease at enrollment and those with heart disease at enrollment obtained a similar magnitude of beneficial reduction in cardiovascular events.

--There was an unusual preponderance of women--69%--unlike most other trials of cardiovascular events. We might therefore argue that JELIS most conclusively showed that benefits of EPA are most confidently demonstrated for females.

--A fish oil preparation containing only EPA was used, rather than the usual EPA + DHA. There are discussions from some corners that argue that DHA is more important than EPA, e.g., algae sources. However, JELIS would argue that EPA does play a role. Is EPA with DHA better, worse, or no different? Unfortunately, there are insufficient data--large, randomized data like JELIS--to help us. Recall that GISSI Prevenzione used a combination of EPA and DHA, as have virtually all other trials examining the effects of fish oil. Also, keep in mind that the epidemiologic observations of the cardiovascular benefits of eating fish suggest that the naturally-sourced omega-3s--a combination of EPA and DHA--are associated with benefit.

--It's surprising that any difference at all was demonstrated, given the high intake of fish in the Japanese. In fact, blood levels of EPA in participants before taking EPA was five-fold higher than in western populations.


One potential difficulty: The study was funded by the manufacturer of the EPA preparation used, Mochida Pharmaceutical Company. We all know what that can do to results.

Nonetheless, the JELIS trial is a study that adds to the emerging wisdom in fish oil.


Copyright 2008 William Davis, MD

Omega-3 MUST be from fish oil

7. March 2008 William Davis (14)
Despite my rants in this blog and elsewhere, at least once a day I'll have a patient say, "I cut back (or eliminated) my fish oil because I get my omega-3s from _______ (insert your choice of flaxseed oil, walnuts, yogurt, mayonnaise, bread, etc.)."

(See prior Heart Scan Blog post: Everything has omega-3.)

When I point out to them that the "omega-3s" in these products are not the same as the EPA and DHA from fish oil, they invariably declare, "But it says so here on the label: 'Contains 200 mg of omega-3 fatty acids'!"

Apparently, some of my colleagues have even endorsed this concept of replacing the omega-3s from fish oil with these "alternatives."

It's simply not true. The linolenic acid that is being labeled as omega-3, while it may indeed provide health benefits of its own, cannot replace the EPA and DHA that fish oil provides.

The most graphic example of the differences between the two classes of oils is in people with a condition called familial hypertriglyceridemia. People with this condition have triglyceride levels of 400, 600, even thousands of mg/dl--very high. Fish oil, usually providing EPA and DHA doses of 1800 mg per day and higher, reduce triglycerides dramatically. A person with a starting triglyceride level of, say, 900 mg/dl, may take 2400 mg of EPA and DHA from fish oil and triglycerides plummet to 150 mg/dl. This person then decides to replace fish oil with a linolenic acid source like flaxseed oil. Triglycerides? 900 mg/dl--no effect whatsoever.

Familial hypertriglyceridemia represents an exagerrated example of the differences between the two oils. Even if you don't have this genetic condition, the differences between the oils still apply.

EPA and DHA are activators of the enzyme, lipoprotein lipase, that accelerates clearance of triglycerides from the blood. Linolenic acid from flaxseed oil, walnuts, and other food sources does not. EPA and DHA block after-eating (post-prandial) accumulation of food by-products that can contribute to coronary and carotid plaque. Linolenic acid does not. EPA and DHA block platelets, reduce fibrinogen, and exert other healthy blood clot-inhibiting effects. Linolenic does not.

The 11,000-participant GISSI-Prevenzione Trial that showed 28% reduction in heart attack, 45% reduction in cardiovascular death with omega-3s used . . . fish oil.

The 18,000 participant JELIS trial that showed 19% reduction in cardiovascular events when omega-3s were added to statin therapy used . . . fish oil. (Actually, in JELIS, they used only EPA wtihout DHA.)

Linolenic acid is not a waste, however. It may exert anti-inflammatory benefits of its own, for instance. But it exerts none of the triglyceride-modifying effects of EPA or DHA.

EPA and DHA from fish oil and linolenic acid from foods each provide benefits in their own way. Ideally, you include both forms of oils--fish oil and linolenic acid sources--in your daily diet and obtain full benefit from each separate class. But they are not interchangeable.


Copyright 2008 William Davis, MD

Osteoporosis and coronary calcium

4. March 2008 William Davis (9)
Several studies over the years have demonstrated a curious paradox:

People with more osteoporosis (thin bones) tend to be more likely to have coronary disease (heart attacks). They also tend to have higher heart scan scores (more coronary calcification as an index of atherosclerotic plaque).

People with more coronary disease and higher heart scan scores tend to have more osteoporosis.


In other words, regardless of which way you tackle the question--osteoporosis first or heart disease first--it leads to the same conclusion: Both conditions are somehow related.

I realize I harp an awful lot on this whole vitamin D issue. But, even after correcting the vitamin D blood levels of many hundreds of people, I remain enthusiastic as ever about the untapped potential of this fascinating factor.

So I couldn't resist showing this amazing comparison of how the long-term effect can be quite graphic.

The first scan is from a 46-year old man and shows normal coronary arteries without calcium and normal density of the vertebra (a common and reliable place to measure bone density).

























The second image is from a 79-year old man with both severe coronary calcification (and therefore severe coronary disease) and severe osteoporosis.
























It makes you wonder if the disordered metabolism of calcium through vitamin D deficiency allows transport of calcium away from bone and into coronaries. This has, however, been shown to not be the case. Instead, they are separate processes, each under local control, but sharing a common pathophysiology (causative factors).

An intriguing question: Would the 79-year old still look like the 46-year old had he begun increasing his vitamin D intake at, say, age 30?

About comment responses and moderation

2. March 2008 William Davis (10)
Just a brief word about my responses to reader comments:

I appreciate the many often insightful and interesting reader comments I receive to the Heart Scan Blog. However, managing them and responding to them has simply become impossible, due to time demands.

I'm afraid that I am unable to answer questions seeking medical advice; this is for your doctor, who knows you and can diagnose and prescribe. I cannot.

I'm also unable to engage in lengthy debates; I've had commenters become very angry when I was unable to engage in lengthy conversations on some topic. Nor am I able to do Google or literature searches for commenters, or review studies, papers, or other materials.

I would urge any readers who wish to engage in in-depth discussions about these issues, talk about lipoproteins, heart disease reversal, etc. to do so on the Track Your Plaque Forums. Yes, it is a fee-for-membership website, a model that has become necessary to pay for the services we provide (not pay me).

I wish that I could answer all the concerns and questions that come my way, but it's simply physically impossible doing so while maintaining a full-time very busy cardiology practice, developing the Track Your Plaque website (which is becoming an enormous responsibility), publishing scientific data, maintaining hospital responsibilities, and spending time with my wife and family. We're all busy and I'm no different. I'm afraid that it's my responses to blog comments that I will have to sacrifice.

I invite commenters to continue to comment on these posts, as I've learned many new things by reading them and find them helpful feedback. And I do read them. Should an especially helpful comment be made, I will feature it in a new blog post, rather than respond directly.

"Flying in the fog"

2. March 2008 William Davis (3)
I received this wonderful response to The Heart Scan Blog post Hammers and Nails:

I am 65 years old. I had a stent inserted in the "widow-maker" artery (80% blockage) a year ago. I had passed out a couple of times (heart rate dangerously low - 30s). I rode to the hospital in an ambulance. Tests revealed short LBBB episodes; mild mitral regurgitation, mild tricuspid regurgitation. Catherization showed 3 vessel CAD. I was told that a medicated stent was absolutely necessary given the situation; regardless, I have to accept that. A pacemaker was installed to prevent bradycardia and keeps heart rate from dropping below 60. I have 20% L distal main blockage and 90% lesion of the high first obtuse marginal at the takeoff. The right coronary had 60% posterior lateral branch stenosis.

Since then I have reduced TG from 360 to 60, LDL from 89 to 82 (although a few months ago it was in the mid-70s), and increased HDL from 30 to 46. I went from 265lbs to 190lbs and hope to eventually get to 180lb this Spring. I did it by progressing from walking to trotting (slow run) and dietstyle changes (low-GI veggies, fruits, etc.) .













On a recent visit the cardiologist said the the LDL needs to be 70 or below to "freeze" the 90% blockage and gave me a prescription for Lipitor. I asked if there were alternatives, like diet, supplements, etc. He admitted that he did not know about those alternative but did know Lipitor. When the only tool you have is a hammer then everything is a nail. I understand that the 90% blockage is important but will not take the Lipitor to achieve the 12 points reduction. Seems like an overkill.

I asked him if there was a way to evaluate my current condition. I was told there was no way. Basically, if I have no symptoms, good. If I have symptoms then it will have to be evaluated. Death could be the only symptom. I swear he was about to say bypass surgery ($$$$$$!) was inevitable. Something is wrong with this "fly-in-the-fog-and-hope-you-don't- hit-a-mountain" approach. Hope is not a strategy!

I am confident that I can reduce LDL to below 70 based on eliminating wheat-products in my diet plus increasing oat bran in my diet. I also take fish oil daily (EPA/DHA-2g). I am looking for a new cardiologist. I just recently purchased your book and find it very instructive. In the meantime I have an appointment with my primary care physician to discuss implementing the Track Your Plaque program. I realize that the one stent will skew the scan numbers but can be used as a baseline number.


Phenomenal weight loss! That alone has likely cut this man's risk in half. But is that it? Is the cardiologist correct--take Lipitor and hope for the best?

Of course not. There are many additional strategies to employ. Eliminating wheat from the diet is an excellent idea: HDL will skyrocket, triglycerides drop even further, small LDL will drop like a stone, blood sugar and blood pressure will drop. He will have more energy, get rid of afternoon energy slumps, sleep better.

He has already added fish oil. If his cardiologist did not mention this, I would say he was guilty of malpractice. The data supporting the addition of fish oil to the treatment program of anyone with heart disease is overhwelming. GISSI Prevenzione: 11,000 participants--28% reduction in heart attack, 45% reduction in death from heart attack. The Japanese JELIS trial of 18,645 participants--19% reduction in dangerous heart events. It's also clear that omega-3 fatty acids from fish oil also compound the benefits of statin agents, should this man choose to begin Lipitor.

Vitamin D brought to normal blood levels is his next "secret weapon" that will further boost his lipids and lipoproteins further into not just "normal" territory, but beyond belief. Even though we aim for 60-60-60 for LDL-HDL-triglycerides in the Track Your Plaque program, adding vitamin D can yield numbers you've never seen before. It's not uncommon, for instance, to see a 10 or 20 mg/dl jump in HDL.

Identify all other hidden causes of coronary plaque. If all the causes have not been fully identified, how can anyone hope to gain full control over coronary plaque growth?

Re: LDL cholesterol of 89 mg/dl at the start. Of course, this is a calculated value, not measured. Because HDL was low and triglycerides high at the start of his program, this means that true LDL--if actually measured--was probably more like 180 to 250 mg/dl, and it was probably nearly all small. So his cardiologist might have advised a helpful treatment, though for the wrong reasons.

Our reader has gone a long way on his own in creating his own prevention program. But there's yet more to do, particularly if the goal is reversal. It is shocking to me that a man like our reader, clearly articulate and motivated, gets virtually no advice beyond "take Lipitor" after all the procedural benefits have been reaped.

Even though one artery can no longer be "scored" due to the presence of the metallic stent, a heart scan would still be invaluable for long-term tracking purposes, just as we advocate in the Track Your Plaque program.



Copyright 2008 William Davis, MD

Goodbye, Dr. Jarvik

29. February 2008 William Davis (0)
HeartWire, the news service of www.theheart.org, posted the following report:

Pfizer pulls Lipitor ads featuring Dr Robert Jarvik in HeartWire

New York, NY - After a series of questions and attacks over its choice of Dr Robert Jarvik to endorse Lipitor in a series of TV commercials, Pfizer has announced that it is withdrawing the ads. As previously reported by heartwire, Jarvik invented the first artificial heart, but he is not a cardiologist, nor does he hold a medical license—factors that drew criticism from detractors and made him and Pfizer a target of a US House Committee on Energy and Commerce investigation into celebrity endorsements in direct-to-consumer advertisements.

In a January 2008 statement, committee chair Rep John D Dingell (D-MI) observed: "Dr Jarvik's appearance in the ads could influence consumers into taking the medical advice of someone who may not be licensed to practice medicine in the United States. Americans with heart disease should make medical decisions based on consultations with their doctors, not on paid advertisements during a commercial break."

Complaints about Jarvik went up a notch this month when the latest ad in the series depicted the inventor rowing a racing scull across a lake, despite the fact that Jarvik himself does not row and the commercial used a body double.

This is typical pharmaceutical industry sleight-of-hand, now you see it, now you don't, that has come to define their policies. And this is just the stuff that comes to light because of some obvious blunders. We can only begin to imagine what sorts of other shenanigans have been swept under the rug, especially adverse effects of drugs that never made it to the light of publication.

Is this just another example of how direct-to-consumer advertising has backfired? I now have patient after patient tell me that they have been so overwhelmed and fed up with TV and magazine ads for drugs that they



Other media outlets have reported that Jarvik was guaranteed $1.35 million for the ads and that Pfizer spent $258 million on Lipitor advertisements between January 2006 and September 2007.

Hammers and nails

28. February 2008 William Davis (4)
I'm sure you've heard the old saying that,

To a man with a hammer, everything looks like a nail.


It couldn't be truer than in heart procedures (the man with the hammer) and heart disease (the nail).

What does it take in 2008 to become an interventional cardiologist trained in all the techniques of angioplasty, stenting, intracoronary ultrasound, etc.? Start with your undergraduate degree (4 years), then medical school (another 4 years), then training in internal medicine (3 years), then general cardiology taining (3 years), then an additional year in interventional cardiology. Each step along the way also involves competing for these spaces, a process that requires much time, money, and sweat.

The total time investment is 15 years after high school. Many if not most college students graduate with debt. Pile on the substantial cost of medical school. Training after medical school pays a modest salary, enough for a single person. Many trainees by then have spouses and a family, would like to buy a house, have bills to pay. (I managed to buy my first house for $69,000 in Columbus, Ohio and paid my mortgage by sleeping only every other night and moonlighting on my off nights.)

By the time the interventional cardiologist-in-training finishes his/her 15 years, they are hungry for a hefty increase in income. After such a time and money investment, I do believe that there is at least some justification for generous income for the years of work involved.

Back to our hammer and nail metaphor. Not only do we now have a man or woman with a hammer, but a really expensive hammer that required a substantial amount of effort to obtain. Now, our hapless hammer-bearer is desperate to see everything in sight as a nail.

You're seen in consultation by this fresh interventional cardiologist in practice for only a few years. Guess what he/she advises? Go straight to the catheterization laboratory, of course. Throw in the fact that insurance reimbursement is most generous for heart procedures, far more than for consulting in the office, doing a stress test, or other simpler, non-invasive tests, and the incentives are clear.

The system, you see, is set up to follow such a path. The path to the cath lab is heavily incentivized, paths in the other direction discouraged, disparaged, or just ignored.

My message: Don't get nailed.

What is abnormal?

27. February 2008 William Davis (1)
What is abnormal?

You'd think that the answer would be easy and straightforward.

However, consider these instances of medical findings that I have witnessed fall repeatedly into the "normal" category:

Diameter of the thoracic aorta: 4.5 cm

Mild coronary plaque by heart catheterization

Carotid plaque of 30-50%


Why isn't a thoracic aorta (the big artery in your chest) of 4.5 cm normal? Because it can be expected to increase in diameter by about 2.5 mm (0.25 cm) per year. Even at its current diameter, it means that stroke risk is greater, since enlarged aortas are diseased aortas that commonly accumulate atherosclerotic plaque with potential to fragment and shower debris to the brain. It means that high blood pressure and/or cholesterol/lipoprotein abnormalities have been uncorrected for years that have allowed the aorta to enlarge.

How about "mild coronary plaque"? Followers of the Track Your Plaque program already know the answer to this one. Mild plaque does not mean mild risk. In fact, most plaques that cause heart attack are mild plaques, not severe blockages. While severe blockages can provide symptom warning and are detected by stress tests, it's the mild blockages that rupture without symptom warning and cause heart attack. So "mild coronary plaque" is no less dangerous than severe coronary plaque.

Likewise, carotid plaque of 30-50%, while it doesn't justify surgery, can grow within just a few years to a severity that allows it to fragment and shower debris to the brain, i.e., a stroke. As with the enlarged aorta, it means that multiple causes of carotid plaque are likely active, including high blood pressure and cholesterol or lipoprotein abnormalities.

Then why would any of these findings be labeled "normal"?

Simple. In the minds of many physicians, if a condition doesn't pose immediate risk, or if it doesn't qualify for surgical "correction," then it is labeled "normal" or "mild."

Thus, an aorta of 4.5 cm cannot justify surgical replacement until it achieves a diameter of 5.5 cm. It is therefore labeled "normal."

"Mild coronary plaque" does not justify insertion of stents or performance of bypass surgery. It must therefore be "normal."

Carotid plaque over 70% is surgically removed, but not 30-50%. 30-50% is therefore "normal."

The tragedy is that many "normal" or "mild" findings, if cast in the proper light, could lead to corrective strategies that could prevent danger long-term or keep surgery from becoming necessary.

The enlarged aorta, for instance, could be stopped and an aneurysm (defined as 5.5 cm or greater) could be prevented, along with dramatically reducing risk for stroke. Carotid plaque, more so than coronary plaque, is a controllable and manipulable condition that should trigger a program of prevention and reversal. Instead, it usually generates advice to have another ultrasound in a year to see if it has yet achieved severity sufficient to justify surgery.

Of course, "mild coronary plaque" is the reason for the Track Your Plaque approach, a chance to seize control over this disease years or decades before procedures are necessary and reduce danger now, not years from now.


Copyright 2008 William Davis, MD

Niacin and hydration

27. February 2008 William Davis (12)
Many people know about niacin's curious effect of the "hot flush," a feeling of warmth that covers the chest and neck, occasionally the entire body.

However, many people are unaware of the fact that hydration can block this effect. In fact, many people who were not advised of this will come to the office describing miserable experiences with niacin--hot flushes that last for hours, intolerable itching, etc.--only to experience little or none of these effects with generous hydration.

The vast majority of the time, two 8-12 oz glasses of water when the hot flush occurs will eliminate the flush within a few minutes.

Sometimes, the hot flush will occur many hours after taking niacin. Nine times out of ten, this delayed effect is also due to poor hydration. For instance, you might be engrossed in your work and forget to keep up with fluid demands. Or, it may be warm and you've lost fluids through sweating. That's when you begin to feel the hot flush creep up on you.

The cure: Lots of water. In this situation, in which you have allowed dehydration to develop, it may require more than two big glasses. Relief from the flush may also take more time, but it still works nearly every time.

On those rare occasions when water by itself is insufficient, then an adult (325 mg), uncoated aspirin or 200 mg ibuprofen can also be used to accelerate relief.

Why go to some much bother? Well, niacin remains the best agent we have for reduction of small LDL, raising HDL (although vitamin D is proving to be a powerful competitor in this arena), and reducing lipoprotein(a). How much do statin drugs contribute to these effects? Very little, if at all.

Several drug manufacturers are also working on "antidotes" to the hot flush effect of niacin that will be packaged within the niacin tablet. Naturally, it will also boost the cost up many times higher.

In the meantime, if or when you experience the niacin hot flush, just think: Put out the "fire" with plenty of water.
All posts by william-davis

More catheterizations would make me happy!

11. October 2006 William Davis (0)
I received this fax today from a cardiologist seeking a position:

"I would prefer to perform as many interventions [stents, angioplasties, etc.] as possible..."

That about sums it up, doesn't it? The goal of this young man, trained in major universities including Columbia University, Harvard, and Emory, is not to pursue an avenue of investigation or healthcare that yields real answers. His goal is to perform as many procedures as possible.

This attitude is deeply ingrained in cardiologists. It's also shared by all procedural medical specialties: the drive to do more and more procedures. It's not because it does more good for the public, but it fulfills a primitive impulse to spread your influence, enlarge your territory, and--of course--make more money.

Personally, I find this impulse repulsive. The fact that this young cardiologist looking for a position is willing to make this statement out in the open demonstrates how widely accepted this attitude is. Imagine your cancer surgeon, looking for a new job, said, "I'm looking to remove as many tumors as I can."

My colleagues have lost sight of the fact that we're trying to reduce or eliminate disease, not enrich our pockets or service some primitive impulse to beat others at our game.

"I hate fish oil!"

9. October 2006 William Davis (1)
I get this comment occasionally, usually from the fishy belching that can occur, rarely because of other crazy effects like rash, fishy body odor, etc.

In the vast majority, fish oil is a benign but wonderfully effective agent. Track Your Plaque followers know that fish oil, starting at 4000 mg per day of a standard 1000 mg capsule preparation, dramatically reduces triglycerides and thereby raises HDL, partially suppresses small LDL, and is the best agent available for reducing postprandial (after eating) abnormalities like IDL and certain VLDL fractions.

However, an occasional person (about 1 in 20) just doesn't like the effects. Are there alternatives? Fish oil packs such a wallop of beneficial effects that can not be replaced by any other single agent or lifestyle practice. For this reason, we have a number of easy strategies to enhance your tolerance for fish oil. (Of course, if your and/or you doctor determine that you're allergic to fish oil, then you should indeed avoid it; thankfully, this is rare.)

Helpful strategies include:

--Refrigerate fish oil capsules--this cuts back on fish belching.
--Take only with meals. This also may increase fish oil's benefits on suppressing after-eating lipoprotein abnormalities.
--Take an enteric-coated preparation--this delays breakdown of the tablet/capsule, making fishy belching less of an issue. Sam's Club has an inexpensive preparation.
--Take liquid fish oil. Usually orange or lemon flavored, liquid fish oil may be a faint fishy taste and odor, but usually not as prominent as the capsules. There's also less stomach upset.
--Coromega--a paste form of fish oil available at health food stores or through http://www.coromega.com. Coromega tastes fruity and comes in little squeeze envelopes.
--Frutol--Pharmax, a British company, makes another fruity fish oil that is non-oily and tastes like apricot. It's actually fairly reasonably priced, too. However, it is hard to find. The only way I know to get is to go online at www.pharmaxllc.com. You may have to actually order through a health care provider.

When using any preparation of fish oil, the best way to determine your dose is to add up the EPA and DHA content. For instance, if you use a fish oil liquid that contains 320 mg EPA and 240 mg DHA per teaspoon, you will need two teaspoons a day to achieve the equivalent of our starting dose of 1200 mg of EPA+DHA, usually provided by 4000 mg total in 4 capsules. Note that some lipid and lipoprotein disorders will require higher doses, e.g., 1800 mg EPA+DHA for high triglycerides (>200 mg/dl) or high IDL.

Sudden death in athletes

6. October 2006 William Davis (0)
A recent report in the Journal of the American Medical Association details how a group in the Veneto region of Italy cut back on the incidence of sudden cardiac death in athletes by a simple screening program.



You can read the abstract of the article at http://jama.ama-assn.org/cgi/content/full/296/13/1593.

Although sudden death in athletes is still a rare event, it is especially tragic when it happens. In this population, the incidence was 3.6 deaths per 100,000 athletes aged 12 to 35 years. By implementing a simple screening program that involved only a physical examination and an EKG, an astounding 89% reduction in sudden death was documented.

What lessons does this hold for those of us interested in coronary plaque reversal? Beyond the obvious lesson of pointing out the great benefit of simple screening of athletes, I believe that it tells us the value of simple screening tools for heart disease in general. It is my strong belief that, if we were to implement CT heart scans among the broad population of men 40 years and over, women 50 years and over--without regard to cholesterol or other relatively lame risk identifiers--we could slash the risk for heart attack and death 90% or more. Putting CT heart scans into the hands of the public makes your coronary risk obvious. It takes the guesswork out of risk predictors like cholesterol and high blood pressure.

But heart scans are already available, you say! Yes, of course they are. But the lack of insurance reimbursement continues to be a restricting factor for many people, despite the number of lives that could be potentially saved and the money that would be saved in the long run by reducing need for major heart procedures. The continuing resistance to prevention by my cardiology colleagues and the persistent ignorance of primary care physicians also remain major impediments.

But it's getting better. You don't have to be chained by ignorance. Put your CT heart scan to good use.

My heart scan was wrong!

6. October 2006 William Davis (0)


Tom came into the office ready for a confrontation.

Tom's wife insisted that he see me to discuss the implications of his CT heart scan score of 459. At age 50, this was clearly bad news that placed Tom in the 99th percentile (worst 1% of men in his age group).

But Tom had already undergone a stress test. There had apparently been a small abnormality, and a heart catheterization had been performed by another cardiologist. "They told me they didn't need to do anything. No stent, no ballon, no bypass, nothing!"

I asked, "Did they tell you that there was any plaque or blockages seen?"

"Yeah, but he said it was nothing. So the heart scan was wrong!"

I've been here many times before. I explained to Tom that, no, his heart scan was not wrong. All the tests he'd undergone siimply provided a different perspective on the same disease. You could say:

--The stress test, being a test of blood flow, may have been abnormal because of the abnormal constrictive behavior of arteries containing plaque, known as "endothelial dysfunction", because the inner lining of arteries (the endothelium) control the tone of the artery. Abnormal constriction in arteries with plaque is quite common.

--The catheterization simply showed that no plaque had collected in a configuration to block flow, thus no stent, etc., since flow was normal. But there was indeed plaque.

All three tests were right; none were wrong. They all provided a little different perspective on the same process. Of course, I favor the heart scan as the means to identify, precisely measure, and track the atherosclerotic plaque in your arteries. The stress test is too crude and only measures flow, the catheterization is not something you'd want to undergo year after year. Catheterization also is too crude a measure to precisely track plaque growth or reversal.

So I explained to Tom that, even though a stent or similar procedure was unnecessary, he remained at substantial risk for heart attack due to plaque "rupture". In fact, Tom's heart attack risk was 5% per year, or approximately 50% over the next decade. That is, indeed, substantial. In fact, you might say that, of the three tests Tom underwent, only the heart scan revealed his true risk.

Fish oil in the news

3. October 2006 William Davis (2)


Hooray for the New York Times. They ran an article pointing out the miserable and inexcusable failure of American physicians to use fish oil after heart attack.

“It is clearly recommended in international guidelines,” said Dr. Massimo Santini, the hospital’s chief of cardiology, who added that it would be considered tantamount to malpractice in Italy to omit the drug.

...in the United States, heart attack victims are not generally given omega-3 fatty acids, even as they are routinely offered more expensive and invasive treatments, like pills to lower cholesterol or implantable defibrillators. Prescription fish oil, sold under the brand name Omacor, is not even approved by the Food and Drug Administration for use in heart patients."

The article focuses on the use of fish oil only after heart attack and doesn't tackle the larger issue of how fish oil is crucial for coronary disease in general. Of course, the article doesn't address the extraordinary effects of fish oil on lipoproteins, particularly triglyceride-containing varieties like VLDL and the postprandial (after-eating) intermediate-density lipoprotein (IDL).

It also talks about prescription fish oil and just glosses over fish oil as a nutritional supplement. I know of few reasons to use the prescription form. More than 90% of the time, nutritional sources of fish oil do the trick. (That is, fish oil capsule supplements, not just eating fish which doesn't provide enough for coronary plaque reduction or control.)

Occasionally, I'll meet someone who has a severe hypertriglyceridemia (very high triglycerides), or is a Apo E 2/2 homozygote (very rare). These special instances may, indeed, do better using prescription fish oil, since it is more concentrated--one prescription capsule providing the same omega-3 fatty acid content as three conventional capsules (1000 mg fish oil, 300 mg EPA+DHA).


But for most of us, the standard fish oil supplement you buy at the health food store or department store does just fine. If you read about the impurity of fish oil supplements (likely prompted by the manufacturer of Omacor, prescription fish oil), refer to the studies by Consumer Reports and Consumer Labs, both of which found no mercury or pesticide residues in dozens of fish oil preparations tested.

Look on the bright side. The conversation is growing. Fish oil, whether prescription or my favorite, Sam's Club Members' Mark brand, is a fabulously effective supplement with benefits that, in nearly all cases, exceeds the benefits of drugs.

Fish oil is an absolute requirement for your Track Your Plaque program and for you to hope to achieve control or reduction of your heart scan score.

Nutritional approaches to homocysteine reduction

3. October 2006 William Davis (0)

For an in-depth discussion of nutritional approaches to homocysteine reduction, see my new article, Nutritional Therapies for Managing Homocysteine , in the most recent issue of Life Extension magazine. You'll find it at:

http://www.lef.org/magazine/mag2006/oct2006_report_homocysteine_01.htm

The report contains a detailed discussion of how to use foods to control homocysteine levels. Though I'm not a homocysteine-crazed fanatic like Life Extension publisher, William Falloon, I still there's some interesting aspects of homocysteine metabolism that need to be explored. I also think there's some genuine benefit to reducing homocystine, preferably with foods, secondarily with supplements.

Also see our recent update on homocysteine on the www.cureality.com website at:
http://www.cureality.com/library/fl_01-006homocysteine.asp

In the update, we tried to make sense of what the new studies on homocysteine treatment, NORVIT and HOPE-2, tell us in light of all the other studies on homocysteine that preceded them.

The American Heart Association diet guarantees you get heart disease!

2. October 2006 William Davis (1)
Perhaps I stated that too strongly.

But the fact remains: the diet advocated by the American Heart Association is awful. The foods endorsed by their approach have no place on a list of healthy foods. Yes, you will find vegetables and fruits, etc.. But you will also find that the 2006 American Heart Association Diet and Lifestyle Recommendations dance around the issue of what foods to avoid. There's no explicit mention of how, for instance, common foods like Shredded Wheat cereal, ketchup, low-fat salad dressings, etc, among thousands of others, should be avoided.

No matter how you time your meals, mix them, combine proteins, fats, and carbohydrates, etc., you simply cannot squeeze health out of products like breakfast cereals, instant mashed potatoes, dried soup mixes, wheat crackers, etc. Yet these are the sorts of foods that are implicitly allowable in the Heart Association's diet program.

You can obtain a little insight into the motivations behind the diet design by looking at the Heart Association's Annual Report list of major supporters:

--ACH Food Companies--maker of Mazola margarine and corn oil. A contributor of between $500,000 and $999,000 to the Heart Association.

--ConAgra Foods--You know them as Chef BoyArdee, Peter Pan peanut butter, Kid Cuisine (pizza, macaroni and cheese). ConAgra contributed between $500,000 and $999,000 to the Heart Association.

--Archer Daniels Midland--Huge worldwide supplier of wheat flours, high-fructose corn syrup, and basic ingredients for manufacture of soft drinks, candies, and baked foods. ADM contributed between $1-4.9 million dollars to the American Heart Association.

Of course, the Heart Association provides many hugely positive services like funding research. But, on many official statements, you need to read between the lines. The Heart Association is funded by industry: medical device makers, drug makers, food manufacturers. Yes, some is contributed in the interest of health. But you can be sure that lots of money is also contributed in the hope of protecting specific commercial interests. Many of those decisions are made behind closed doors or on the golf course.

Be skeptical. Just because the Heart Association diet is a Casper Milquetoast version of a health program, it does not mean that you have to subscribe to their watered-down, politically correct, and downright useless nutrition recommendations.

I'm just right!

2. October 2006 William Davis (1)
Ben is an energetic 45-year old entrepreneur. He started his own security alarm company and has, with tremendous hard work and long hours, built it into a successful local business. Despite his long hours, he found time to coach his son's football team and help with raising his 3 kids.

Ben's life took a detour when he had urgent bypass surgery at age 39. Just three years later, the chest pains and fatigue he'd experienced before bypass returned. Another heart catheterization revealed that all of his bypass grafts except one had closed. Three stents were implanted to salvage his original coronary arteries.

That's when I met Ben. Shockingly (perhaps I should know by now!), Ben was taking Lipitor and had been advised to follow a low-fat diet. That was the full extent of his heart disease prevention program. The burning question that I wanted answered was "Why did a 39-year old man have heart disease?".

Our analysis uncovered a smorgasbord of hidden patterns. You name it, Ben had it: postprandial (after-eating) patterns like IDL, low HDL, and, most notably, small LDL and lipoprotein(a). That's why Ben had heart disease as a 39-year old man--plain and simple.

We proceeded to correct all of his patterns. But the one aspect of his program that he struggled with: weight. At 5 ft 9 inches, Ben started at 285 lbs before bypass. He did manage to get to 270 after his surgery. I told him that, if he was going to get full control of his small LDL pattern, he needed to get to <210 lbs, perhaps even lower. Without substantial weight loss, he would never seize full control over coronary plaque.

Ben was satisfied that we had identified the hidden causes of his heart disease. But he remained skeptical that that magnitude of weight loss was necessary. Built like a football player, he looked stocky but not outright fat. He got down to 240 lbs but then he decided that he looked too skinny and just went right back up to 250-260 in weight.

At a weight of 250, this puts Ben's BMI (body mass index) at around 37, way over the cut-off of 30 for obesity. Now, the BMI can be misleading in people with larger frames and more muscle. But Ben undeniably had a generous abdomen, encasing the visceral fat that drives small LDL.

Unfortunately, Ben remained skeptical until I put three more stents into his right coronary artery last evening.

Small LDL is a powerful activator of lipoprotein(a). In other words, there's something peculiarly evil about the combination of small LDL and lipoprotein(a) that brings out the worst in both. You can't correct just one or the other. You've got to correct both. Don't learn this lesson the hard way.

I think (hope) that Ben is on track to get to around 200 lbs.

Prevention: Bad news in bits and pieces

30. September 2006 William Davis (1)
Jan clearly did not want to talk about her heart scan. Her score of 502 came as a shock to her. After all, she'd survived breast cancer just a year earlier, having been through dozens of radiation treatments, chemotherapy, not the mention the emotional upheaval.

Now I was telling Jan that she had a very high heart scan score with a heart attack risk of 5% per year. Then we got to her lipoprotein patterns: Jan had several striking abnormalities, including a misleading LDL cholesterol that underestimated her true LDL by nearly 100% (LDL particle number), small LDL, and the dreaded lipoprotein(a).

"I can't handle this! Why did I get the stupid scan in the first place?!"

Giving her a chance to collect her emotions, I discussed how, even though this business can be frightening, it's far--FAR--better than the alternative: heart attack at 3 am, rush to the hospital, stents, bypass surgery, etc. Or, death for the >30% of people who don't make it to the hospital in time.

That's why I often tell people that prevention of disease is bad news in bits and pieces. But it's a lot more manageable this way. Coronary plaque is a controllable process. You don't have much control in the midst of a heart attack.

A second chance

29. September 2006 William Davis (1)
Stewart had a CT heart scan in 2004. Score: 475.

As always in the Track Your Plaque program, Stewart had his lipoproteins assessed. Among his patterns were LDL 157 mg/dl, severe small LDL, and the (post-prandial, or after-eating) IDL. Stewart was also "pre-diabetic" with a blood sugar of 123 mg/dl. Blood pressure was also a major issue. Although initially concerned, life and distractions got in the way, and Stewart's attentions drifted away.

Two years of a lackadaisical effort and Stewart's heart scan score was 600, a 26% increase. Not as bad as it could have been doing nothing (i.e., 30% per year), but still far from great. But, even with the increase in score, we still really didn't get Stewart's attention. He went about his business with a very lax dietary program, overindulging in breads, crackers, goodies, hot dogs, etc., and following a virtually non-existent exercise program except for playing golf once or twice a week.

Unfortunately, Stewart started having pains in his chest with very minimal efforts like climbing a single flight of stairs. His stress test proved abnormal. Stewart then received a stent in his left anterior descending coronary and another in his circumflex. His right coronary artery had a 40-50% blockage, close to requiring a stent.

I stressed to Stewart that this had been preventable. Should motivation remain unchanged, the next step would be bypass surgery.

I think I finally succeeded in getting Stewart's attention. He found the prospect of a bypass operation a lot more concrete than the idea of progression or regression of coronary plaque. So Stewart is being given a second chance. Unfortunately, we will no longer be able to track Stewart's plaque very effectively, since two of three arteries now contain stents, and only the right coronary remains scorable.

I hope Stewart succeeds. But I sure wish he had done this earlier. He had realistic hopes of never requiring stents or bypass surgery.

Learn from Stewart's mistakes. Attention to your program requires vigilance. You can't ignore the causes of your coronary plaque for any length of time without it catching up to you. But seize your first and best chance.

Fat Head: Tom Naughton's manifesto for low-carb eating

12. March 2010 William Davis (16)
I just got back from Jimmy Moore's low-carb cruise to the Bahamas.

Among the many interesting people I met on the cruise was the creator of the documentary film, Fat Head, Tom Naughton.

Tom brings both creative insights into low-carbohydrate eating as well as humor. Low-carb eating can be a pretty contentious issue, but Tom made it fun. He will make you laugh about many of the odd notions we have about diet.

Among the best parts of Fat Head is Tom's portrayal of the effects of carbohydrates on insulin and fat metabolism:






Fat Head joins the ranks of films like Food, Inc, that make nutrition information entertaining. For anyone interested in a unvarnished look at diet, weight loss, along with a few laughs along the way, Tom Naughton's Fat Head is worth viewing.

Oatmeal: Good or bad?

11. March 2010 William Davis (67)

You've heard it before: oatmeal reduces cholesterol. Oatmeal producers have obtained permission from the FDA to use a cholesterol-reducing claim. The American Heart Association provides a (paid) endorsement of Quaker Oats.

I've lost count of the times I've asked someone whether they ate a healthy breakfast and the answer was "Sure. I had oatmeal."

Is this true? Is oatmeal heart healthy because it reduces LDL cholesterol?

I don't think so. Try this: Have a serving of slow-cooked (e.g., steel-cut, Irish, etc.) oatmeal. Most people will consume oatmeal with skim or 1% milk and some dried or fresh fruit. Wait an hour, then check your blood sugar.

If you are not diabetic and have a fasting blood sugar in the "normal" range (<100 mg/dl), you will typically have a 1-hour blood glucose of 150-180 mg/dl--very high. If you have mildly increased fasting blood sugars between 100 and 126 mg/dl, postprandial (after-eating) blood sugars will easily exceed 180 mg/dl. If you have diabetes, hold onto your hat because, even if you take medications, blood sugar one hour after oatmeal will usually be between 200 and 300 mg/dl.

This is because oatmeal is converted rapidly to sugar, and a lot of it. Even if you were to repeat the experiment with no dried or fresh fruit, you will still witness high blood sugars in these ranges. Do like some people and pile on the raisins, dried cranberries, or brown sugar, and you will see blood sugars go even higher.

Blood sugars this high, experienced repetitively, will damage the delicate insulin-producing beta cells of your pancreas (glucose toxicity). It also glycates proteins of the eyes and vascular walls. The blood glucose effects of oatmeal really don't differ much from a large Snickers bar or bowl of jelly beans.

If you are like most people, you too will show high blood sugars after oatmeal. It's easy to find out . . . check your postprandial blood sugar.

In past, I recommended oat products, specifically oat bran, to reduce LDL, especially small LDL. I've changed my mind: I now no longer recommend any oat product due to its blood sugar-increasing effects.

Better choices: eggs, ground flaxseed as a hot cereal, cheese (the one dairy product that does not excessively trigger insulin), raw nuts, salads, leftovers from last evening's dinner.

Mustard: Super health food?

6. March 2010 William Davis (32)
Could mustard--yes, the yellow condiment you smear on hot dogs--be a super heart healthy food in disguise?

Consider that mustard contains:

Vinegar

Turmeric

No appreciable sugar


The vinegar slows gastric emptying, resulting in slower absorption of any carbohydrates and a reduced glucose area-under-the-curve. Of the little fats contained (about 3 grams per 1/4 cup), most are desirable monounsaturates. Mustards are relatively rich in selenium, with 20 mcg per 1/4 cup, helpful for protection against cancer and thyroid disease, and magnesium, 31 mg per 1/4 cup.

Turmeric is added to most mustards. One of the constituents of turmeric, curcumin, the substance that confers the bright yellow color, has been a focus of interest for its anti-inflammatory effects. Curcumin has been documented to reduce activity of the inflammatory enzymes cyclooxygenase-2 (COX-2), lipoxygenase, and reduce activity of inflammatory signal molecules, tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1,2,6,8, and 12, and monocyte chemoattractant protein (MCP). Curcumin also has been shown to reduce LDL oxidation, a potentially important step in atherosclerotic plaque formation. Turmeric is used as a tea by Okinawans. (Hmmmm . . . )

Turmeric content of mustard can vary, of course. Likewise, sugar content. Look for mustards that are not sweetened, so avoid honey mustard in particular. Look for hot, brown, horseradish, Dijon, etc. If there is a downside to mustard, it's sodium content, though the 709 mg per 1/4 cup should only be a problem for those who are sodium-sensitive (African Americans, in particular).

So perhaps mustard isn't exactly a super health food. But it may have some bona fide health effects and should be used generously especially if you are concerned about blood sugar and inflammatory phenomena.

Exercise and blood sugar

5. March 2010 William Davis (30)
There is no doubt that exercise yields benefits across a spectrum of health: reduced blood pressure,  reduced inflammation, reduced blood coagulation, better weight control, stronger bones, less depression, reduced risk for heart attack.

Exercise also influences blood sugar. Diabetics understand this best: Exercise reduces blood sugar 20, 30, 50 or more milligrams. A starting blood sugar, for instance, of 160 mg/dl can be reduced to 80 mg/dl by jogging or riding a bicycle. (I recently had brunch at an Indian restaurant with my family. Blood sugar one-hour postprandial: 134 mg/dl. I was sleepy and foggy. I got on my stationary bike and pedalled at a moderate clip for 60 minutes. Blood sugar: 90 mg/dl.)

Could the reduction of blood sugar with exercise be THE reason that exercise and physical activity provide such substantial benefits?

Think about it. Reduced blood sugar:

1) Reduces risk for future cardiovascular events.
2) Reduces glycation of proteins, i.e., reduced glucose binding to proteins like the ones in artery walls and the lenses of your eyes.
3) Reduces blood coagulation
4) Reduces endothelial dysfunction (abnormal artery constriction that leads to atherosclerosis)

This might explain why it doesn't require high levels of aerobic activity to derive benefit from exercise, since even modest efforts (e.g., a 15-minute walk after eating) reduce blood sugar substantially.

The incredible 33-year, 18,000-participant Whitehall study tells us that a postprandial (after-eating) blood sugar of an impossibly-difficult 83 mg/dl is required to erase the excess cardiovascular risk of blood sugar. Could this simply be telling us that physical activity or exercise is required to suppress blood sugars to these low levels?

It makes me wonder if an index of the adequacy of exercise is your post-exercise blood glucose.

The most important weight loss tool

4. March 2010 William Davis (15)

Question: What is the most effective tool available to help you lose weight? 


A pedometer (walk 10,000 steps, etc.)?

A treadmill? 




A bicycle?






No. None of the above. 

The most important tool you can use to achieve weight loss is your glucose monitor:



Timing of blood sugars

3. March 2010 William Davis (5)
Because different foods generate different blood sugar (glucose) responses, the timing of your blood sugar is an important factor to consider.

This question has come up a number of times. Commenters have asked whether the one-hour postprandial glucose is timed with the start of the meal or the conclusion of the meal.

In my view, if we simply ignored all aspects of meal composition, then blood glucose should be obtained one hour after the conclusion of a meal. This is because most mixed meals (i.e., mixed in composition among proteins, fats, and carbohydrates) yield peak blood glucose levels at 60-90 minutes after consumption. Timing blood glucose to 60 minutes after the conclusion of a meal puts the sample right about at the peak.

But this is an oversimplification. For instance, here is the blood glucose behavior after so-called "complex" carbohydrates wheat bread, rye bread, rye made with beta glucan, and whole wheat pasta (50 grams carbohydrates each) in slender, healthy volunteers, mean age 29 years:


From Juntunen et al 2002

Note that blood glucose peaks at 35 minutes postprandial. (To convert glucose in mmol/L to mg/dl, multiple by 18. Thus, whole wheat bread increased blood glucose from 94 mg/dl to 122 mg/dl. Also note the lower peak glucose for pasta, but sustained higher glucose levels hours later.)

In another study, older (mean age 64 years), overweight (BMI 27.9) females with diabetes were given 50 grams carbohydrate, 50 grams carbohydrate with olive oil, or 50 grams carbohydrate with butter:


From Thomsen et al 2003. Control meal of soup plus 50 g carbohydrates ({blacktriangledown}), the control meal plus 80 g olive oil ({circ}), and the control meal plus 100 g butter (•).

In this experience, note that postprandial glucose peaks 60-120 minutes after the meals (consumed within 10 minutes), delayed more when either oil is included. Blood glucose started at 144 mg/dl and peaked as high as 230 mg/dl with carbohydrates only; peaks were reduced (along with AUC) when oil was included. (Note the differential effect, olive oil vs. butter.)

These two sets of observations give you a range of blood glucose behavior. One side lesson: Carbohydrates should never consumed by themselves, else you will pay with a high blood sugar (not to mention the hypoglycemic response later for many).

Psssst . . . There's sugar in there

1. March 2010 William Davis (13)
You non-diabetics who check your postprandial blood sugars already know: There are hidden sources of sugar in so many foods.

By now, everybody should know that foods like breakfast cereals, breads, bagels, pretzels, and crackers cause blood sugar to skyrocket after you eat them. But sometimes you eat something you thought was safe only to find you're showing blood sugars of 120, 130, 150+ mg/dl.

Where can you find such "stealth" sources of sugars that can screw up your postprandial blood sugars, small LDL, inflammation, blood pressure, and cause you to grow visceral fat? Here's a few:

Balsamic vinaigrette
Many commercially-prepared balsamic vinaigrettes, especially the "light" varieties, have 3 or more grams carbohydrates per tablespoon. Generous use of a sugar-added vinaigrette can therefore provide 12+ grams carbs. (Some, like Emeril's and Wish Bone, also contain high-fructose corn syrup.)

Hamburgers
I learned this lesson the hard way by taking my blood sugar after having a hamburger, turkey burger, or vegetarian burger (without bun): blood sugar would go way up. The effect is due to bread crumbs added to the meat or soy.

Tomato soup
If it were just tomatoes, it would still be somewhat high in sugars. But commercially-prepared tomato soup often contains added high-fructose corn syrup, sucrose, and wheat flour, bringing sugar totals to 12 to 20+ grams per half-cup. A typical 2-cup bowl of tomato soup can have upwards of 80 grams of sugar.

Granola
Sure, granola contains a lot of fiber. But most granolas come packed with sugars in various forms. One cup of Kellogg's Low-fat Granola with Raisins contains an incredible 72 grams (net) carbohydrates, of which 25 grams are sugar.


Given modern appetites and serving sizes, you can see that it is very easy to get carried away and, before you know it, get exposed to extraordinary amounts of sugar and carbohydrates eating foods you thought were healthy.

And don't be fooled by claims of "natural" sugar. Sugar is sugar--Just check your blood sugar and you'll see. So raw cane sugar, beet sugar, and brown sugar have the same impact as white table sugar. Honey, maple syrup, and agave? They're worse (due to fructose).

How low should blood sugar be?

28. February 2010 William Davis (0)
What should your blood sugar (glucose) be after eating?

Take a look at the data from the Whitehall study reported in 2006. The Whitehall Study stands apart from other studies in that it was very large (over 18,000 participants) who were observed for an unusually long time (33 years). All participants were administered a 50 gram glucose "challenge" at the start with glucose levels checked after the glucose challenge.

Here's what they found:




From Brunner et al 2006.