What role cholesterol medication?

10. aprilie 2006 William Davis (0)
A frequent conversation point among my patients, as well as participants in the www.cureality.com program, is "Are cholesterol medications really necessary?"

No, they are not. What IS necessary is to correct all manifest and hidden causes of coronary plaque. Among these causes, in my view, is LDL cholesterol of 60 mg/dl or greater. There are many other causes of coronary plaque--e.g., small LDL particles, unrecognized hypertension, Lp(a), hidden diabetic patterns, etc.--but reducing LDL to 60 mg is still an important part of a plaque-reversing effort.

Insofar as we wish to get LDL to this goal, the statin cholesterol drugs like Lipitor, Zocor, Crestor, etc. may play a role. However, they should only be considered after a full effort dietary program is pursued. Don't follow the American Heart Association's diet unless you want to fail. It's nonsense.

For a more detailed discussion of how to use nutrition and nutritional supplements to reduce LDL cholesterol, go to www.lef.org, the website for the Life Extension Foundation. I wrote an article for their magazine called "Cholesterol and Statin Drugs: Separating Hype from Reality". You'll find the article at http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=1295&query=davis%20cholesterol%20natural&hiword=CHOLESTEROLA%20CHOLESTEROLS%20DAVI%20DAVID%20DAVIE%20DAVIES%20DAVIN%20DAVIO%20DAVISON%20DAVISS%20DAVIT%20NATURALBASED%20NATURALES%20NATURALIZED%20NATURALLY%20NATURALS%20NATURE%20NATURES%20cholesterol%20davis%20natural%20.)

Can your plaque-reversal efforts succeed without statin drugs? It depends on your causes. For instance, someone with small LDL and Lp(a) only may do great on our basic program and then add niacin. Unfortunately, another person with a starting LDL cholesterol of 240 mg/dl--sky high--will have more success with these drugs.

Believe me, I am no blind supporter of drug companies and their flagrantly profit-seeking practices which, in my view, are cut-throat, shoving anyone and anything out of their way to increase profits and market share. I share many of Dr. Dave Warnarowski's views on how vicious their tactics can be; see his recent Blog post at http://www.drdavesbest.com/blog/ called "I smell a rat".

Nonetheless, the deep and well-funded research of the pharmaceutical industry does yield some useful tools. You don't have to love the insect exterminator, but if your house is being eaten by termites, his services can be useful. Same thing with these drugs. Useful--not the complete answer, not even close, but nonetheless useful in the right situations. Sometimes antibiotics are necessary, even life saving. That's how cholesterol drugs are, too.

Take it all in the proper perspective. Your goal is not cholesterol reduction, per se, but plaque control, preferably reversal.

Supplement Mania!

9. aprilie 2006 William Davis (3)
Ever hear of "polypharmacy"? That's when someone takes too many medicines. People will have lists of 15-20 prescription medicines, for instance, with crazy interactions and oodles of side-effects.

Well, how about "poly-supplments"? That's when someone takes a large number of nutritional supplements.

Let me tell you about a 45 year old man I met.

In an effort to rid himself of risk for heart disease that he felt was likely shared with his family (brother and father diagnosed with heart attacks in their late 40s), Steve followed a program of nutritional supplementation. You name it, he took it: hawthorne, anti-oxidant mixtures, vitamins C, E, B-complex, saw palmetto, 7-keto DHEA, velvet deer antler, gingko biloba, policosanol, chronium picolinate, green tea, pine bark extract, St. John's Wort, CoEnzyme Q10, papain and other digestive enzymes...He became a distributor for a nutritional supplement company to allow him to afford his own extraordinary program.

To satisfy himself that he had indeed "cured" himself of heart disease, he got himself a CT heart scan. His score: 470, in th 99th percentile. Steve's heart attack risk based on this score was around 10% per year. High risk, no question.

For weeks after his scan, Steve admitted walking around in a daze, not knowing what to do. Years of telling himself that he had effectively dealt with his heart disease risk, now all down the drain.

When we met, I persuaded him that to think that this collection of supplements would reverse heart disease was magical thinking. We trimmed his list down to the essentials and got him on the right track.

Heart disease is controllable and reversible, but not this way. Don't fool yourself into thinking that some collection of supplements will be enough to stamp out your heart disease risk. Just like taking an antibiotic when you don't have an infection achieves nothing, so does taking the wrong supplements.

What does heart scanning mean to you?

8. aprilie 2006 William Davis (0)
CT heart scans can mean different things to different people.


What does a heart scan mean to you? There are several possibilities:

1) A way of reducing uncertainty in your future.

2) A tool to crystallize your commitment to health.

3) A device to help you track how successful your heart disease prevention program is.

4) A trick to get you in the hospital.

5) A moneymaking tool for unscrupulous physicians hoping to profit from "downstream" testing, particularly heart catheterizations.


Like anything, heart scans can be used for both good and evil. How can you be sure that your heart scan is put to proper use--for your benefit and not someone else's profit?

Simple: Get educated. Understand the issues, be armed with informed questions.

If, for instance, you're a 55-year old female with a heart scan score of 90, active without symptoms, and you're told to have a heart catheterization right off the bat---run the other way. This is bad advice. A heart procedure like catheterization at this score in an asymptomatic woman is very rarely necessary. That decision can only be made after a step-by-step series of decisions are made by a truly interested, unbiased party. (A stress test is almost always required in this situation before the decision can be made to proceed with a catheterization.)

Unfortunately, in 2006, getting unbiased advice from your doctor is still a struggle. That's why we started Track Your Plaque---unbiased information, uncolored by drug or device company support, with an interest in the truth.

Coronary disease is drying up!

7. aprilie 2006 William Davis (1)
I had an interesting conversation with a device representative this morning. He was a sales representative for a major medical manufacturer of stents, defibrillators, and other such devices for heart disease.

Since I'm still involved with hospital heart care and cardiac catheterization laboratories, this representative asked me if I was interested in getting involved with some of the new cardiac devices making it to market over the next year or two. "The coronary market is drying up, what with coated stents and such. We've got to find new profit sources."

Well, doesn't that sum it up? If you haven't already had this epiphany, here it is:

HEART DISEASE IS A PROFITABLE BUSINESS!

Why else can hospitals afford billboards, $10 million dollar annual ad campaigns, etc.? They do it for PROFIT. Likewise, device and drug manufacturers see the tremendous profit in heart disease.

The representative's comments about the market "drying up" simply means that the use of coated stents has cut back on the need for repeat procedures. It does NOT mean that coronary disease is on the way out. On the contrary, for the people and institutions who stand to profit from heart care, there's lots of opportunity.

Track Your Plaque is trying to battle this trend. Heart disease should NOT be profitable. For the vast majority of us, it is a preventable process, much like house fires and dental cavities.

Mammogram for your heart

6. aprilie 2006 William Davis (0)
With the booming popularity of "64-slice CT scans", there's a lot of mis-information about what these tests provide.

These tests are essentially heart scans with added x-ray dye injected to see the insides of the arteries. However, to accomplish this, a large quantity of radiation is required. In addition, the test is not quantitative, that is, it is not a precise measure that can be repeated year after year.

It is okay to have a 64-slice CT coronary angiogram. It is NOT okay to have one every year. That's too much radiation. However, a heart scan can be repeated every year, if necessary, to track progression or regression. Once stabilization (zero change) or reduction is achieved, then you're done (unless your life takes a major change, like a 20 lb weight gain).

The tried-and-true CT heart scan is the gold standard--easy, inexpensive, precise, and repeatable. Not true for 64-slice angiograms.

Is your doctor using "leeches"?

4. aprilie 2006 William Davis (0)
What if you went to your doctor for a problem and he/she promptly placed leeches on your body?

Yeccchhhh! Would you go back? I'd bet that you'd run the other way as fast as your bleeding legs could take you. Outdated health practices like "bleeding" are outdated for good reason.

Then why would you allow your doctor to approach your heart disease prevention program by checking cholesterol and then waiting for symptoms to appear? That miserable approach leads to tragedy and death all too often--ask Bill Clinton! He might as well have had leeches!

Don't allow your doctor's ignorance or disinterest impede your prevention program. Get your coronary plaque measured, then attack it from all sides by knowing all causes, hidden and obvious. That's why Track Your Plaque is such an effective program.

I often wonder why more doctors aren't using this unbelievably powerful approach to deal with heart disease. But when I see colleagues implanting stents, defibrillators, and the like for many thousands of dollars per patient, the answers are obvious. Given a choice of a rational, effective program of prevention that pays the doctor a few hundred dollars for his time, versus $2000 to $10,000 for a procedure, you can see that the temptation is irresistible for many physicians.

All in the family--What to do if there's heart disease in your family

3. aprilie 2006 William Davis (0)
What should you do if a close relative of yours is diagnosed with coronary disease?
This question came up recently with a patient of mine. The patient--a strapping, 47 year old businessman who looked the absolute picture of health--was undergoing bypass surgery. Although I'd met him for the purposes of plaque reversal, he was already having symptoms and his stress test was flagrantly abnormal, all discovered after a heart scan score of 765. On the day after the patient's bypass, the patient's brother came to me. Understandably concerned about his own health, he asked what he should do. The answer: get a heart scan.
Measure the disease with the easiest test available. If his heart scan score is zero, great--he's at exceptionally low (near zero) risk for heart attack. A modest program of long-term prevention is all that's necessary. What if his score is like his brother, should he get in line for his bypass? No, absolutely not! But he will need two things: 1) a stress test to ascertain whether or not he's safe (60% likelihood a stress test would be normal), and 2) an effort to determine how the heck he got so much plaque. (We favor lipoprotein testing, of course, for greatest diagnostic certainty.)
Message: Learn from the lessons your own family provides. Don't let this valuable information go to waste.
Cureality | Real People Seeking Real Cures

Condition Afflicts Millions: Do you have “YBS”?

12. May 2014 Lisa G Nutrition (0)
After one of the harshest winters, spring has finally arrived.  The welcomed warmer temperatures and longer daylight hours infuse us with a sense of renewal and new beginnings.   Low and behold we begin to come out of hibernation and start the mad dash to engage in positive lifestyle changes such as eating better, exercising, proper sleep and taking appropriate nutritional supplements.  But invariably, life happens.  

Yep, just when you were about to get started, it happens.  YBS sets in.   I see this “condition” all too often with clients attempting to enter or re-enter into any number of behavior changes.  I will go so far as to say we all have been afflicted at one point or another in our lives.  I call this condition Yeah But Syndrome, or “YBS”.    It is often paralyzing and prevents those afflicted from moving into action, instead remaining in a state of inertia.  

There are many symptoms of YBS but the following are some of the most common.  

• Yeah I planned to go to the gym today BUT, the kids needed a ride to practice.  
• Yeah I really want to eat better BUT I don’t have the time.   
• Yeah I didn’t plan to eat the cake BUT my husband wanted too, so I did also.   
• Yeah I really meant to go to the grocery shopping BUT I was too tired, so I hit the drive- thru.  
• Or this is a good one. Yeah I meant to start today BUT, I’ll start tomorrow.  

But tomorrow never comes.  You get the drift.  We can all come up with a million yeah buts, in other words, excuses.    The good news is the treatment for YBS is simple--just do it!  Take action.  The reality of today’s 24-7 planet is there will always be something.  The kids, work commitments, family obligations and various projects that need your attention will perpetually be present in some shape or form.  The difference to make the difference is to learn to dance in the rain, not wait for the rain to pass.  When will all the stars align so that your world will be “just right” to start?  If not NOW, WHEN will you begin?  

The key word here is begin.   Far too frequently, I coach clients that shoot themselves in the foot before they start.   Instead of consuming yourself with all the barriers to entry, select reasonable, low-hanging fruit that is “doable.”    The art of lifestyle change is to avoid all-or-nothing thinking and begin to appreciate what you CAN do, versus focusing energy on what you can’t do.  What is one action you can do TODAY to move toward your wellness goal(s)?  Start to focus on what you can do in the mist of your existing life demands. This mantra is a friendly reminder: BE-DO-HAVE.  Be committed.  Do what it takes.  And you will have results.  

Lastly, if you think removing cereal from your morning routine it is too difficult and you can’t do it. Guess what-- you’re likely right.   What you think is what you get!   But what if you think instead, “I can do this.  There are many truly healthy options for breakfast to replace cereal such as eggs and veggies that will help me look and feel my best.”  Then guess what--you will!  This simple change in mind-set can start a tidal wave of change and prevent you from abandoning ship when life tosses you into rough waters.  Ongoing support is hugely important to sustain lifestyle changes.  Join the conversations in the Cureality Forum to engage the support of health coaches and Cureality Members to stay on track. 

We Need More.....Kettlebell

8. May 2014 Amber B Exercise (0)
You either love them or you hate them.

When you are in love with kettlebells, like I am, you enjoy the multi-muscle group movements.  Kettlebell workouts are fluid, like a dance, putting together a chain of movements that leave your heart pounding and sweat pouring.  Yes, there’s some sneaky cardio component to a kettlebell workout.   A great blend of aerobic and anaerobic conditioning.

If you hate kettlebells it’s because kettlebell exercises keep you honest with proper exercise execution.  Form is imperative to moves like the kettlebell swing or the kettlebell snatch.  Do it incorrectly and you’ll be either sore or have bruised wrists the next day.  But this is no reason to shy away from the kettlebell.  You have way too much to gain from this odd looking piece of exercise equipment.  

You will get a mega -caloric burn.  The American council on Exercise states that the average kettlebell workout burns 20 calories per minute.  That’s 1200 calories in just one hour.   Kettlebell workouts utilize many muscle groups to give you an efficient, total body conditioning workout.  

If you’re looking for a toned back side get a kettlebell.  The classic kettlebell swing works all the posterior muscles like your glutes, hamstrings, and lower back.  But only if you use correct form.  Otherwise you'll find yourself with nagging back pain, instead of a better butt.  

Kettlebell exercises are functional movements that will allow you to play hard without getting injured.  If you are an athlete, a nature enthusiast, or just want to keep up with the kids then you need to give kettlebells a try.  During a workout, the exercises will target movements that will make getting up and down off the floor easier, as well as bending over to pick something up.

If you are interested in doing kettlebell workouts start with a coach or take class.  You can’t fake form with kettlebell exercises or you could end up hurt.  I’m not trying to scare anyone away because good form is easy to learn.   Your body will memorize the correct movement pattern and you’ll be on your way to a successful kettlebell workout.  

Thyroid and the gut: Hidden health partners

8. May 2014 Chris K Thyroid (0)
Though I have personally dealt with both auto-immune thyroiditis (Hashomoto’s) and several gut issues (wheat sensitivity, gastritis, etc.), it was not until recently that I discovered how close the thyroid and gut work together to keep you healthy – and how problems with one can affect the other along with your overall health.
 
Most of us understand that the primary function of the gut, that 25 to 30 feet of “tubing” that includes everything from your stomach to your large intestines, is to process the food we eat and allow the “good stuff” (essential nutrients) to pass into our blood stream while keeping the “bad stuff” (harmful proteins) out. However, it may surprise some that the gut also holds as much as 70% of all the immune tissue in the body.
 
Now, imagine all the health havoc that could ensue if, suddenly, the gut stopped doing its job – particularly if it failed to stop toxic proteins from entering the blood stream and then mounted an overzealous immune response against them.  Sometimes, those overzealous immune responses reach beyond their intended targets to attack otherwise healthy tissues and organs – like the thyroid gland.
 
Recent studies indicate that thyroid hormones play a significant role in maintaining gut integrity, preventing leaky gut that can, in some cases, lead to auto-immune attacks against the thyroid.  A properly functioning gut also aids the production of thyroid hormones by converting some of the inactive “T4” thyroid hormone into the functional “T3” hormone.  Failure to simultaneously maintain both a healthy gut and a healthy thyroid can create a vicious cycle leading to chronic health problems and declining vitality.
 
What it all means is that to enjoy optimal health, you must promote good thyroid health to promote good gut health and vice versa.  Unfortunately, traditional medicine tends to focus on one issue to the exclusion of others.  A typical endocrinologist may treat your under active thyroid without spending a moment to address underlying gut issues.  A gastroenterologist will work alleviate a gut problem but will rarely address a potential thyroid problem.
 
This illustrates, once again, how our bodies work as a system and why it is necessary to bridge the “healthcare gaps” in traditional medicine by becoming personally responsible for your health.  I encourage everyone to consult the Cureality Program Guide and online Cureality Diet and Thyroid Health Tracks to learn more about how to optimize both your gut and thyroid health on your journey to realizing complete, whole-body health.

Omega-3 fatty acids likely NOT associated with prostate cancer

18. July 2013 William Davis Omega-3 fatty acids (6)
A weakly constructed study was reported recently that purportedly associated higher levels of omega-3 fatty acid blood levels and prostate cancer. See this CBS News report, for instance.

Lipid and omega-3 fat expert, Dr. William Harris, posted this concise critique of the study, exposing some fundamental problems:

First, the reported EPA+DHA level in the plasma phospholipids in this study was 3.62% in the no-cancer control group, 3.66% in the total cancer group, 3.67% in the low grade cancer group, and 3.74% in the high-grade group. These differences between cases and controls are very small and would have no meaning clinically as they are within the normal variation. Based on experiments in our lab, the lowest quartile would correspond to an HS-Omega-3 Index of <3.16% and the highest to an Index of >4.77%). These values are obviously low, and virtually none of the subjects was in “danger” of having an HS-Omega-3 Index of >8%. So to conclude that regular consumption of 2 oily fish meals a week or taking fish oil supplements (both of which would result in an Index above the observed range) would increase risk for prostate cancer is extrapolating beyond the data.

This study did not test the question of whether giving fish oil supplements (or eating more oily fish) increased PC risk; it looked only a blood levels of omega-3 which are determined by intake, other dietary factors, metabolism and genetics.

The authors also failed to present the fuller story taught by the literature. The same team reported in 2010 that the use of fish oil supplements was not associated with any increased risk for prostate cancer. A 2010 meta-analysis of fish consumption and prostate cancer reported a reduction in late stage or fatal cancer among cohort studies, but no overall relationship between prostate cancer and fish intake. Terry et al. in 2001 reported higher fish intake was associated with lower risk for prostate cancer incidence and death, and Leitzmann et al. in 2004 reported similar findings. Higher intakes of canned, preserved fish were reported to be associated with reduced risk for prostate cancer. Epstein et al found that a higher omega-3 fatty acid intake predicted better survival for men who already had prostate cancer, and increased fish intake was associated with a 63% reduction in risk for aggressive prostate cancer in a case-control study by Fradet et al). So there is considerable evidence actually FAVORING an increase in fish intake for prostate cancer risk reduction.

Another piece of the picture is to compare prostate cancer rates in Japan vs the US. Here is a quote from the World Foundation of Urology:

"[Prostate cancer] incidence is really high in North America and Northern Europe (e.g., 63 X 100,000 white men and 102 X 100,000 Afro-Americans in the United States), but very low in Asia (e.g., 10 X 100,000 men in Japan).”

Since the Japanese typically eat about 8x more omega-3 fatty acids than Americans do and their
blood levels are twice as high, you’d think their prostate cancer risk would be much higher...
but the opposite is the case.

Omega-3 fatty acids are physiologically necessary, normalizing multiple metabolic phenomena including augmentation of parasympathetic tone, reductions of postprandial (after-meal) lipoprotein excursions, and endothelial function. It would indeed make no sense that nutrients that are necessary for life and health exert an adverse effect such as prostate cancer at such low blood levels. (Recall that an omega-3 RBC index of 6.0% or greater is associated with reduced potential for sudden cardiac death.)

I personally take 3600 mg per day of EPA + DHA in highly-purified, non-oxidized triglyceride form (Ascenta Nutrasea liquid) that yields an RBC omega-3 index of just over 10%, the level that I believe the overwhelming bulk of data suggest is the ideal level for humans.

Are statins and omega-3s incompatible?

18. June 2013 William Davis (4)
French researcher, Dr. Michel de Lorgeril, has been in the forefront of thinking and research into nutritional issues, including the Mediterranean Diet, the French Paradox, and the role of fat intake in cardiovascular health. In a recent review entitled Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?, he explores the question of whether statin drugs are, in effect, incompatible with omega-3 fatty acids.

Dr. Lorgeril makes several arguments:

1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.

2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.

He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association's advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.

In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:

--Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.)
--Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.)
--Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)

Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?

I fear we don't have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.



DHA: the crucial omega-3

22. May 2013 William Davis (5)
Of the two omega-3 fatty acids that are best explored, EPA and DHA, it is likely DHA that exerts the most blood pressure- and heart rate-reducing effects. Here are the data of Mori et al in which 4000 mg of olive oil, purified EPA only, or purified DHA only were administered over 6 weeks:



□ indicates baseline SBP; ▪, postintervention SBP; ○, baseline DBP; •, postintervention DBP; ⋄, baseline HR; and ♦, postintervention HR.

In this group of 56 overweight men with normal starting blood pressures, only DHA reduced systolic BP by 5.8 mmHg, diastolic by 3.3 mmHg.

While each omega-3 fatty acid has important effects, it may be DHA that has an outsized benefit. So how can you get more DHA? Well, this observation from Schuchardt et al is important:

DHA in the triglyceride and phospholipid forms are 3-fold better absorbed, as compared to the ethyl ester form (compared by area-under-the-curve). In other words, fish oil that has been reconstituted to the naturally-occurring triglyceride form (i.e., the form found in fresh fish) provides 3-fold greater blood levels of DHA than the more common ethyl ester form found in most capsules. (The phospholipid form of DHA found in krill is also well-absorbed, but occurs in such small quantities that it is not a practical means of obtaining omega-3 fatty acids, putting aside the astaxanthin issue.)

So if the superior health effects of DHA are desired in a form that is absorbed, the ideal way to do this is either to eat fish or to supplement fish oil in the triglyceride, not ethyl ester, form. The most common and popular forms of fish oil sold are ethyl esters, including Sam's Club Triple-Strength, Costco, Nature Made, Nature's Bounty, as well as prescription Lovaza. (That's right: prescription fish oil, from this and several other perspectives, is an inferior product.)

What sources of triglyceride fish oil with greater DHA content/absorption are available to us? My favorites are, in this order:

Ascenta NutraSea
CEO and founder, Marc St. Onge, is a friend. Having visited his production facility in Nova Scotia, I was impressed with the meticulous methods of preparation. At every step of the way, every effort was made to limit any potential oxidation, including packaging in a vacuum environment. The Ascenta line of triglyceride fish oils are also richer in DHA content. Their NutraSea High DHA liquid, for instance, contains 500 mg EPA and 1000 mg DHA per teaspoon, a 1:2 EPA:DHA ratio, rather than the more typical 3:2 EPA:DHA ratio of ethyl ester forms.

Pharmax (now Seroyal) also has a fine product with a 1.4:1 EPA:DHA ratio.

Nordic Naturals has a fine liquid triglyceride product, though it is 2:1 EPA:DHA.





Krill oil: Do the math

21. May 2013 William Davis (0)
The manufacturers of krill oil claim that the phospholipid form of omega-3 fatty acids, EPA and DHA, enhance their absorption. There are indeed some data to that effect:


Here are some representative krill oil preparations available on the market:


MegaRed Krill Oil:
EPA 50 mg
DHA 24 mg
Total omega-3s (EPA + DHA + other forms) 90 mg
Price: $28.99 for 60 softgels

Source Naturals (a fine company otherwise, by the way):

EPA 150 mg
DHA 90 mg
Total omega-3 fatty acids 300 mg
Price: $24.99 for 60 softgels

Alright, let's do some simple math:

Average volume of blood in the human body (all components): 5000 cc
Percentage of red blood cells (RBCs) by volume: 45%
Total volume RBCs: 2250 cc
Percentage of total volume RBCs occupied by fatty acids:

What tests are MORE important than cholesterol?

12. May 2013 William Davis (8)
In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.

So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.


All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Cranberry Sauce

21. November 2012 William Davis (3)
Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque!

Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.

There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.

1 cup water
12 ounces fresh whole cranberries
Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía)
1 tablespoon orange zest + juice of half an orange
½ cup chopped walnuts
1 teaspoon ground cinnamon
½ teaspoon ground nutmeg
¼ teaspoon ground cloves

In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.

Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.

Transfer mixture to bowl, cool, and serve.


Apple Cranberry Crumble

18. November 2012 William Davis (0)
Apple, cranberry, and cinnamon: the perfect combination of tastes and scents for winter holidays!

I took a bit of carbohydrate liberties with this recipe. The entire recipe yields a delicious cheesecake-like crumble with 59 “net” grams carbohydrates (total carbs – fiber); divided among 10 slices, that’s 5.9 grams net carbs per serving, a quantity most tolerate just fine. (To reduce carbohydrates, the molasses in the crumble is optional, reducing total carbohydrate by 11 grams.)

Other good choices for sweeteners include liquid stevia, stevia glycerite, powdered stevia (pure or inulin-based, not maltodextrin-based), Truvía, Swerve, and erythritol. And always taste your batter to test sweetness, since sweeteners vary in sweetness from brand to brand and your individual sensitivity to sweetness depends on how long you’ve been wheat-free. (The longer you’ve been wheat-free, the less sweetness you desire.)


Crust and crumble topping
3 cups almond meal
1 stick (8 tablespoons) butter, softened
1 cup xylitol (or other sweetener equivalent to 1 cup sugar)
1½ teaspoons ground cinnamon
1 tablespoon molasses
1½ teaspoons vanilla extract
Dash sea salt

Filling
16 ounces cream cheese, softened
2 large eggs
½ cup xylitol (or other sweetener equivalent to ½ cup sugar)
1 Granny Smith apple (or other variety)
1 teaspoon ground cinnamon
1 cup fresh cranberries

Preheat oven to 350° F.

In large bowl, combine almond meal, butter, sweetener, cinnamon, molasses, vanilla, and salt and mix.

Grease a 9½-inch tart or pie pan. Using approximately 1 cup of the almond meal mixture, form a thin bottom crust with your hands or spoon.

In another bowl, combine cream cheese, eggs, and sweetener and mix with spoon or mixer at low-speed. Pour into tart or pie pan.

Core apple and slice into very thin sections. Arrange in circles around the edge of the cream cheese mixture, working inwards. Distribute cranberries over top, then sprinkle cinnamon over entire mixture.

Gently layer remaining almond meal crumble evenly over top. Bake for 30 minutes or until topping lightly browned.
What are "normal" triglycerides?

What are "normal" triglycerides?

12. April 2011 William Davis (67)
Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.
Tags :

Comments (67) -

  • Stephan Guyenet

    4/11/2011 6:58:50 PM |

    Hi Dr. Davis,

    I searched for that reference but I wasn't able to find it.  I found two papers from Austin et al. in 2000 but neither contained that graph.  Would you mind giving a more detailed reference for it?  I'd like to have that paper as a reference.  Thanks!

  • Anonymous

    4/11/2011 7:14:14 PM |

    HI Dr. Davis--

    Since I have been having my cholesterol levels checked, my triglyceride level has always been on the very low side...ave. around mid 30's.  My hdl  and ldl are generally around low to mid 80's.

    Could you say something about the people who have low triglycerides...is this healthy or a concern?

    My doctors usually think this is great , but I wonder.
    Thank you.

  • Dr. William Davis

    4/11/2011 9:40:20 PM |

    Hi, Stephan--

    Here's the URL for the abstract on Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/2372896

    I also see that I got the year wrong: It was 1990. (Now corrected.)


    Anon--

    Low triglycerides are wonderful. Your values are at the biologically perfect range.

  • Anonymous

    4/11/2011 10:07:10 PM |

    This is from Anon , who wrote you about my very low triglycerides-in the 30's.  Thank you so much for responding--I had been concerned there was something wrong with me!  
      
    I do not think my levels are due to genetics as my siblings have cholesterol issues. I think it is my diet and ex.

    Do you see many people with tri's in the 30's?  
    Thanks again!

  • Frank Hagan

    4/11/2011 10:13:07 PM |

    I must be doomed; even with vlc diet (less than 30g per day), fish oil and niacin, my triglycerides have never been under 103. They started at 440, so that's progress, but I suspect I have familial hypertriglyceridemia, as I can't get them to budge lower after two years.

    I tried going off niacin at one point, and they rose to 140 again. So I continue with the fish oil (1200mg of EPA and 900mg of DHA), niacin (1500mg 1x day) and vlc diet.

  • Might-o'chondri-AL

    4/11/2011 10:36:00 PM |

    Triglyceride (Trig.)clearing relys on the enzyme lipo-protein lipase being able to function at the capillary endothelium. If a Trig can get into a cell it is not taken out of circulation.

    Trigs move around in the circulation bound to lipo-proteins, and one natural component (among several components) of the lipo-protein molecules that carry Trigs is identified as Appoliprotein (Apo) C III. When there is an un-naturally high proportion  of Apo C III involved  this inhibits the working of the enzyme lipo-protein lipase, which is an essential enzyme for clearing Trigs from the blood stream (note: this is not discussing how Trigs get formed).

    Apo C III blocks the lipo-protein lipase enzyme from functioning at the capillary endothelium; Apo C III doesn't actually bind to the lipo-protein lipase enzyme.  It (the enzyme) can't get to work at that capillary inter-face when Apo C III over-abundant; so, there is less lypo-lysis (ie: Trig cleaving off) done to the Trig carrying lipid molecules (ie: VLDL, IDL and chylomicron lipids burdened with Trigs).

    So, what complicates the natural process when there is no underlying genetic cause obstructing Trig clearing from the blood stream ? If you said "insulin" you are correct; insulin signaling has a distinct regulatory affect on the APOC3 gene expression, which encodes for Apo C III.

    Docs interventions keep Trigs down in the obvious manner of setting up less substrate for Trig formation. What contiues to intrigue me is how insulin is involved in metabolic signalling beyond text book role of "driving" glucose into cells.

  • Might-o'chondri-AL

    4/11/2011 10:39:55 PM |

    edit last comment (mine) 1st paragraph, 2nd sentence to read:
    " If a Trig can NOT get into ...."

  • Anonymous

    4/11/2011 11:05:37 PM |

    When I had my last lipid analysis, I had been fasting for about 36 hours.  I frequently do intermittant fasting. My numbers were very contradictory and I wonder if my LDL levels were artificially increased due to the extended fast. My triglycerides were 69, VLDL were too few to be measured, but the number of small LDL particles was very high.  Thank you for addressing this issue.

  • Harry

    4/11/2011 11:21:54 PM |

    might, as I understand it, as VLDL loses trigs, it becomes IDL, and after further loss of trigs and all apolipoproteins except ApoB, it becomes LDL. I have been wondering if receptors in the LDL family are part of the process whereby VLDL and IDL and LDL lose trigs to cells throughout the body. Is this the way it works, or are receptors of the LDL family all or  mostly in the liver?

  • Adam Michael

    4/11/2011 11:35:42 PM |

    Anonymous, would you mind sharing your typical diet and lifestyle practices, including exercise?  I'm sure all curious minds could benefit!  Thank you.

  • Anonymous

    4/12/2011 1:11:53 AM |

    Adam M--In response to your question about my regimen. There really is nothing extreme about it so I have been baffled for years with my cholesterol results esp. the tri's in the 30's.

    For the past 20 yrs. I have almost totally avoided processed foods.Basically no junk food at all. Most of that time I ate no red meat. I have probably not eaten enough food...I  have always been a light eater and on the thin side. Lowish bmi but def. not anorexic or any eating disorder . I haven't eaten butter, though I do drink no-fat, or low fat milk and eat yogurt  daily as well. I use olive oil as much as I care to have, and eat walnuts and almond butter.I don't drink alcohol except on the very rare occassion--maybe a few times a yr.

    No special supplements...but fish oil over the past 8yrs. and a good level vit d. for the past few years. I was probably vit d deficient most of my life before supplementing vit d.


    For the past 10 years, I have walked briskly at least 6 days a week 4-6mi. I lift weights  (dumbbells #15-3-4 days a week. Do some tai chi.

    So you can see ...nothing too special but I do think vastly different than most Americans.

    My guess is that I am reaping the benefits of some good habits from the past 20 plus years. As I said my siblings take bp meds and statins....I don't take either. I think they have bad eating habits, don't exercise consistently and drink alcohol . Though 2 siblings have fairly decent diets, don't drink much and still need a statin and bp meds.

    I am female in my late 50's and siblings a bit older and a bit younger, male and female.

    Hope this helps. Anon.

  • Might-o'chondri-AL

    4/12/2011 1:12:10 AM |

    Hi Harry,
    The liver exports most Trigs bound to VLDL; when measuring fasting Trigs these are mostly complexed to VLDL. IDL (intermediate density lipo-protein) is really a spin off phase of a VLDL remnant, and is itself short lived (ie: IDL degrades quickly).

    When measuring fed (post-prandial) Trigs these are some appearing in VLDL (ie: liver exported) and some Trigs the chylo-microns carry (ie: from the intestine, a different source of Trigs); a relatively minor amount would be Trigs carried by IDL. When fasting (ex: overnight) there are very sparse amounts of Trigs associating with chylo-microns and IDL would be neglibible.

    HDL also has to carry Trigs; it (HDL) brings them back to the liver, which hydrolizes (cleaves) those Trigs for the liver to "play" with again. The HDL Trigs are not scavenged from the long enduring VLDL lipo-protein; but are Trigs HDL had picked up (ie: from the peripheraly circulating short lived IDL & chylo-microns).

    My understanding is that it is not the LDL receptors that are key to how & when Trigs physically get "off" of any molecule that is carrying a Trig. The Apo C III (detailed previously) is one of several proteins ( Apo C molecules exist in different iso-forms, do so simultaneously and sometimes as mutations); a lot of sub-groups get "bundled" to the Apo B complex.

    Apo C III component having excessive expression is what interfers with the enzyme  (lipoprotein lipase) involved in cleaving off Trigs. LDL receptor dynamics only add mitigating circumstances to how/where/when a circulating Trig is coming to be (or not be) presented for cleaving off.

  • Paul

    4/12/2011 3:00:41 AM |

    At least 50% of my caloric intake consists of fat, mostly saturated and monounsaturated from grass-fed tallow, ghee, butter, cheese, coconut, olive oil, almonds, avocados, and one tsp. fish oil... I get plenty from organ meats, wild salmon, free-range eggs, chicken, and beef too.  Not to mention I avoid grains, starch, and sugar as though they are poison.

    I'm a 50 y.o. male, and try to perform at least three apposing compound weight resistant exercises every day (bench-presses, pull-ups, squats, military-presses, rows, lunges, dead-lifts, power-cleans, or clean-&-jerks.)

    I've been doing this for a couple years.

    Along with very (visibly) favorable body comp muscle/fat ratios, my last 12 hr. triglyceride measurement came in at 52 mg/dl.  I think I'll stick with what I'm doing.

  • Rick

    4/12/2011 3:15:34 AM |

    Dr Davis,

    I'm a bit confused about number 4. You suggest that a postprandial value of greater than 88 is dangerous, but accept levels of up to 90 in your program. Are you sure the figures are correct?

    Also, are the 4 points in the order you intended?: you move from fasting triglycerides being too high (1), to being low (2), then to being too high again (3), then you move to non-fasting triglycerides in 4, starting with quite a very low figure (88), and suddenly jumping to 400+. How about more typical non-fasting figures in the 100+ or 200+ ranges?

  • Anonymous

    4/12/2011 5:35:26 AM |

    I must really be screwed. Even on six fish oil caps a day and a gram of niacin, I'm at 292.. my all time low was 157. I'm on even more fish oil and cut out breakfast cereal and other sources of high fructose corn syrup. What I need is a whole new genotype....

  • Alex

    4/12/2011 6:00:44 AM |

    Dr. Davis,

    While I understand that your target audience are probably Americans, as a European, I would be very grateful if you would also post values of the tests you speak of in the measurements used on the other side of the Atlantic. Here we speak of triglycerides in mmol/L, not in mg/dl, so whenever I read your posts I have to sit here with a conversion sheet and calculator, and considering that I can't make notes on other people's websites, I have to do so EVERY time I read your posts, even for the second or third time. It would be very helpful (and probably not too much work for you) if you could post values in both measurement systems, so I can put down the calculator and conversion sheet in the future and put all my attention to the contents.

    Thanks for listening.

  • LifeCoachAndy

    4/12/2011 7:38:17 AM |

    To ' I must be screwed up, VLC diet may be working for , so you  may want to try a different approach, eg. low fat plant based diet, do some fasting, also may need some attention to your liver.

  • Anonymous

    4/12/2011 8:44:10 AM |

    @Alex: +1

    Australia uses mmol/L also as it's the SI standard.

    Perhaps a converter on your site or quick reference table?

  • majkinetor

    4/12/2011 11:20:59 AM |

    "I must really be screwed. Even on six fish oil caps a day and a gram of niacin, I'm at 292.. "
    If you didn't do this, you may try exercising, sesame butter and soy lecithin.

    @Alex:
      +1
    We need M measure too. I have to convert each read, too.

  • Medicomp INC.

    4/12/2011 3:58:11 PM |

    Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

    Interesting point. Many people think that fat is the most important part of a diet to assess, other factors definitely play a role in heart complications.

  • Might-o'chondri-AL

    4/12/2011 4:43:59 PM |

    Exertion (ex: manual work, breathing harder exercising, endurance training, etc.) improves insulin resistance; the
    sedentary, overweight, obese and Type II diabetics are told to actively exercise. Less insulin lingering in circulation means less insulin signals to ratchet up the Apo C III level; Trigs can clear out of circulation (as detailed above).

    Lipo-protein lipase enzyme can then robustly cleave of circulating Trigs for then getting into cells. In the cell the Trig must be processed into a "droplet" molecule for storing inside the cell; up to 1% of our genome is suspected to be involved in the biochemistry of achieving fat "droplet", which reflects it's importance.

    Fat Storage-Inducing Transmembrane Protein (FITM) in the cell's endoplamic reticulum make this conversion of Trigs into droplets (again note: this is not how Trigs are initially assembled). FITM uses the enzyme di-acyl-glycerol O-transfer-ase
    to do the job; then the droplet is rendered into the storage form called di-acyl-glycerol.

    FITM 1 is what exists in skeletal muscle endoplasmic reticulum to make muscle stores of di-acy-glycerol. When we exert ourselves and run out of glucose to burn the muscle takes back off the acyl-CoA fractions
    from stored di-acyl-glycerol; then it cobbles back together tri-acyl-glycerol molecules (note: this is the same molecule as a tri-glyceride, the more commonly used term just skips mentioning the acyl group) to burn and meet the demand for energy.

    Quite conveniently, for those who exert themselves, sustained activity also induces more di-acyl-glycerol transferase enzyme production; it is positive feed back augmenting the rate at which muscles can access their stored "fat" to burn (ie: training increases endurance).

    With muscle fitness burning up the on site reserves of di-acyl-glyceride the muscle can then take up more Trigs from the blood stream. Thus Trigs readings are lower for most geno-type individuals who regularly exert themselves (there are a few instances, mostly disease related, where low circulating Trigs are due to the liver holding on to too many Trigs).

    Our fat (adipose) cells' endoplasmic reticulum are the other site of a lot of lipid droplet processing for storage; there the adipose cells use FITM 2. When there is no exertion (ie: muscle cells have made no room for more stored di-acyl-glycerides) the Trigs slowly  get into the adipose cells(and some other tissues); so for the sedentary individual burning off that fat "reserve" is extremely difficult.

  • Harry

    4/12/2011 5:40:24 PM |

    Might, have you seen Mendivil's paper "Metabolism of VLDL and LDL containing apolipoprotein C-III and not other small apolipoproteins" It's at

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818784/

    It seems to me that there must be some docking involved when a VLDL or LDL particle sheds trigs either in the liver or elsewhere in the body. Maybe it's not receptors of the LDL family that do the docking, but as I understand it, lipoprotein lipase isn't carried by the ApoB containing lipoprotein, but rather, is a component of the receiving cell that facilitates transporting the trigs through the receiving cell wall. The process may not involve full endocytosis, where the whole ApoB-containing particle is engulfed by the cell, but it seems to me that there must be some sort of adhesive or attractive region on the cell to trap the VLDL or LDL at least for a while so that the trig can be unloaded. Any idea how this works?

    From what I've read, it appears that the longer half-life of LDL in the circulation, vs that of VLDL and IDL, is due to ApoE being contained in VLDL and IDL, but not LDL. Since ApoE can attach to LDL receptors as well as or better than ApoB can, this results in more rapid clearance of VLDL and IDL than LDL.  

    As a result of this discussion and some references like Mendivil's paper, it appears that ApoC is involved also. Since LDL carries only ApoB, maybe that also contributes to the longer half-life of LDL.

    Might, have you considered joining Dr. Davis' Track Your Plaque (TYP) forum? I'm a member, and we have many interesting discussions of CHD issues. There is a small fee involved, but we discuss many things before they make it into the Heart Scan Blog. For example, we discussed the subject of this blog thread about a year ago, and as a result, I purchased a cardiochek meter and did a postprandial trig test. My fasting trig level was 57, and I then drank 6 oz of heavy cream. My trigs peaked 4 hours later at 69, which showed that my low-carb diet (30 g/day) had acclimated me to rapid removal of trigs. We learn a lot from each other's experiences.

    Anyway, your knowledge of cellular and molecular processes would make a great addition to the TYP forum. There are a number of ApoE3/4, E2/4, and E4/4 people there as well as E3/3's, and We sometimes discuss posts you have made in other fora. I hope you will consider joining us. And by the way, I'm not connected in any way with the TYP forum other than being a member who likes to get into the nitty gritty of CHD issues.

  • Renfrew

    4/12/2011 6:40:45 PM |

    Might o'chondria:

    I am enjoying your posts, though they are quite technical and mostly go over my head. It seems you are a very knowledgeable contributor here.
    I have one request: You'd be of service for many, if you could add some "behavioral" recommendations or at least sensible things to do/to avoid after you analyze/report/explain physiological parameters and biochemical findings.

    A simple sentence, like: Because of this, it would make sense to do this... or that.... or avoid this...would be much appreciated.
    Thanks.

    Renfrew

  • Might-o'chondri-AL

    4/12/2011 7:47:20 PM |

    Hi Renfrew,
    This is Dr. Davis' blog so it is my feeling that specific health
    recommendations be his; and he does make them (some here & apparently more specifics  elsewhere). I am not a medical doctor, and do not follow
    all his recommendations (as I know them)for that matter.

    The fancy words I use are there because contemporary science has coined them to describe the complex details researchers keep finding. A lot of the hyphens (ex: "...-...-...") in words are inserted by me; this breaks up technical words into their component parts. I chose to do this so readers might identify some of the key parts  researchers coined that word from and not just tune out because of the jargon.

  • Brent

    4/12/2011 8:26:47 PM |

    To Frank Hagan (I Must Be Doomed) and Anon (I Must Be Screwed) - It does not seem like either of you take enough fish oil.  I visited Doc a month ago and he moved me from 2,400 mg DHA & EPA per day up to 3,000 mg per day - and I my Trigs were in the upper 70's.  Have not tested since.

    My understanding of TYP dosages is that you start around 3000 mg per day (DHA & EPA) and you go up from there, as high as 6,000 mg per day until your triglycerides are under 60.

  • Renfrew

    4/12/2011 8:53:45 PM |

    Whatever happened to KRILL OIL ? Has it been forgotten?

    I have read that KRILL oil is far more bioavailable than fishoil and chemically more stable, thus less prone to go rancid. Also because we are talking about phospholipids here which are absorbed much btter than ordinary fishoil, I would assume KRILL is the better choice.
    Unfortunately there does not seem to be much science on this. Probably because big pharma cannot make a buck out of this.
    I'vew been taking Krill oil for a year now and my trigs went from 250 to 56 in about 1 month. Stable since then. Unfortunately it does not seem to reduce LDL or raise HDL.
    Any experience, comments or details on KRILL?
    Renfrew

  • Ensues

    4/12/2011 9:58:35 PM |

    Hi Frank-

    I am exactly the same way.  Mine started over 1000 then to 769.  On fish oil, VLC, and Tricor (200mg) the lowest I have been able to achieve is 229.  My HDL is very low <25.  Neither of my parents have issues.  Very frustrating.  I am hoping my body/metabolism is healing and it my tri's will come down with time.

  • Ellen

    4/12/2011 10:06:13 PM |

    Hey Anon-- you ain't the only one! my triglycerides are always around 31. I always thought they were too low as well because they flag low for the lab range.

  • Paul Mcgrath

    4/12/2011 10:14:34 PM |

    @Renfrew

    No offense, but Might-o's valuable contributions here are clear to me on what specific behavior would be a healthy one.

    It can be summed up in one word... move. Well, maybe two more words would be clearer... lift something.  You would literally have to be blind and deaf not to notice all the effective programs  to help reach your goals. I particularly love Erwin Le Corre's Movnat - http://movnat.com/

    Our distant ancestors didn't have cars, automated climate controlled houses, refrigerators, cooking stoves, grocery stores, TV's, computers, game consoles, or various other modern conveniences that relieved or distracted them from having to go do physical work... just to survive.

    Combine that with today's widely available, tasty, cheap high carb food sources, you have a perfect synergistic formula for diseases of western civilization.

  • Anonymous

    4/12/2011 10:55:41 PM |

    MCA:

    You are my bochemistry reference guide and I really appreciate your posts. Please keep posting because you have the ability to answer why.
    Moving ones body has got to be one of the best investments in physical and mental health. I would rather do that then obsess or stress-out about numbers on a lab test. Get out in the woods and mountains and cover a lot of miles. I am fortunate because I live in Montana and have the wilderness in my backyard.

  • Might-o'chondri-AL

    4/12/2011 11:33:19 PM |

    10 mg/dl  =    0.555 mmol/L
    10 mmol/L =  180.0   mg/dl

    Maybe this scale of 10s will help those who need to do quick conversions.

  • Anonymous

    4/13/2011 2:08:11 AM |

    Put me in the genetically hopeless camp.  Tri's are 150 despite vegetables being my only source of carbs and intense activity 3 x's per week (about 1.5 hrs total), body fat and natural musculature that could have me as a paleo-bod model.  I feel hopeless on the blood lipid front.

  • michael goroncy

    4/13/2011 5:43:17 AM |

    Easy to confuse....
    Chol.LDL&HDL are on a different scale than TRIGS.
    To convert mmol/l to mg/dl multiply by 39 for cholesterol.
    For TRIGS multiply by 89.

  • Anonymous

    4/13/2011 12:34:20 PM |

    @Might-o'chondri-AL said...
    " 10 mg/dl = 0.555 mmol/L
    10 mmol/L = 180.0 mg/dl"

    When you are doing molar conversions there is a different factor for every chemical. Glucose, triglycerides, ...whatever. All have VERY different figues.

  • Anonymous

    4/13/2011 12:46:46 PM |

    Since removing bread and starch from my life my values have never been so good.  I do *very* occasionally have some rice or soaked beans or lentils...but my fasting triglycerides were 33, my total cholesterol 221, my HDL was 94 and LDL 121.  Just posting in case you are collecting data Smile

  • Anonymous

    4/13/2011 1:15:52 PM |

    My fasting triglyceride level fell from 81 to 46 over a 9 month period.  During this time, I doubled my exercise from 30 mins a day to 60 mins a day (every day of the week).  I believe that this is the cause.  For those trying to cut out animal fat, I have to report that I eat chicken skin and pork fat and this does not affect my cholesterol levels.

  • Stargazey

    4/13/2011 2:07:01 PM |

    I think Might-o'chondri-AL was giving us the conversion factors for glucose.

    My triglycerides went from 118 pre-Atkins to 43 after a few years on it. No change in exercise; I just cut out the carbs.

  • Might-o'chondri-AL

    4/13/2011 3:10:33 PM |

    Thanks M. Goroncy & Stargazey,
    for correcting my mistake; I do make them, so anytime welcome errors being pointed out.

  • Geoffrey Levens

    4/13/2011 4:13:21 PM |

    "Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role."

    I exercise moderately daily, HIIT and resistance. Eat Fuhrman's ETL diet so I get about 30% calories from fat (raw nuts and seeds)and get about 250-300 grams carbs per day (zero refined carbs though).  My fasting trigs just read at 56.  High dose fish oil can elevate trigs, refined carbs also. Not so much apparently for whole foods, unrefined carbs.

  • Eric

    4/13/2011 4:38:58 PM |

    Well stated Paul Mcgrath!

  • Travis

    4/13/2011 9:43:17 PM |

    Dr. Davis,

    2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

    I have lower fasting triglycerides since going on a low carb, higher protein and fat diet similar to what you suggest (they dropped from about 100-120 to 60-90). Yet, when I've had an NMR Lipoprofile done, it shows that I have high amounts of small LDL particles (in particular 850 nmol/L of small LDL-P and 1720 nmol/L LDL-P). I'm disappointed both that my triglyercides don't seem to be consistently low and that my small LDL-P is high. I'm otherwise healthy, not obese, no signs of insulin resistance, and eat primarily meat, eggs, dairy, and leafy green vegetables (with some starchy vegetables and fruit).
    I recognize you suggest this may be partly genetic, but what does this mean for me and is there anything I can do about it? Have you written about this elsewhere that I can't find? Thanks!

  • Eric

    4/13/2011 10:25:49 PM |

    Travis- This might help ApoE.

    ApoE 4/4 have to be more selective in their fat selections and amounts than an Apo 3/3.

    This may be just 1 genetic marker that can account for your numbers.

  • Adam

    4/14/2011 1:07:53 PM |

    2 years ago, when I had a case of the flu, and it didn't go away for 3 months, my doc ordered me a blood panel. My fasting triglycerides were 240mg/dL.

    Of course, i also suffered from the typical symptoms of metabolic syndrome: high BP, high cholesterol, obesity (40" waist), diabetic level of fasting blood glucose, low HDL... He told me to eat more "healthy whole grains" and cut out all fat and eat no red meat, to which I answered "that is exactly how I have been eating for decades!"

    Google then revealed to me Marks Daily Apple, I cut out all forms of sugar, grains, legumes, partially hydrogenated oils, and most dairy. Added in more grassfed beef, wild fish, coconut. Exercise sessions are short but as intense as physically possible.

    2 years later, I'm 40kg (88lbs) lighter, my waist is now 29" (smaller than my mom and I'm a man!), no more high BP, no more high cholesterol, HDL is 90+mg/dL.

    Triglycerides? 38mg/dL.

    Good thing I didn't listen to my doctor and take a heap of pills which he said I have to take for the rest of my life.

  • Steve

    4/14/2011 1:59:16 PM |

    Fascinating NYTimes article (4/13): "Is Sugar Toxic" by Gary Taubes. LINK

  • Frank Hagan

    4/14/2011 2:00:02 PM |

    Brent, thanks for the comment re: fish oil dosage. I am at 3,900mg of EPA&DHA combined (specifically 2400mg of EPA and 1500mg of DHA).

    I have a blood test coming up in June; I may increase to 5,200 mg to see if that has more effect.

  • Frank Hagan

    4/14/2011 2:07:07 PM |

    Ensues, you might check with your doctor about using niacin (not sure if there's an issue taking it with Tricor so I would check with him; I couldn't continue on Tricor due to an allergic reaction to it).

    My lowest triglyceride reading was when I was combining VLC, fish oil at 3,900mg EPA & DHA daily and 1,500mg of niacin.

    Dr. Davis has a lot of info here on niacin, including recommendations for using SloNiacin (over the counter) instead of the prescription version (Niaspan, I think) to save money. And he has some tips to avoid the flusing most of us get (what works for me is a regular aspirin 30 minutes before taking the niacin, and drinking plenty of water.)

  • Anonymous

    4/14/2011 7:35:37 PM |

    I notice some comments about large doses of fish oil (3+ grams daily) in order to reduce triglycerides.

    Any concerns over immune suppression at these doses? Or even 1-2g doses?

    I recall one pubmed study showing close to a 50% reduction in NK activity at a rather paltry EPA dose of 720mg/daily.

    http://www.ncbi.nlm.nih.gov/pubmed/11237929

    3+gm of fish oil might scare me a bit, longterm, if that study is correct.

  • Tim Tom

    4/14/2011 8:44:56 PM |

    I agree with your last statement that carbohydrates are a much bigger culprit to high triglyceride levels than fat intake. Looking forward to that post.

  • Dash

    4/15/2011 5:32:32 AM |

    Thank you for all of this information, it was really helpful for one of my classes.

  • Might-o'chondri-AL

    4/15/2011 5:53:06 AM |

    Hi Annon,
    NK, a type of lymphocyte cell, is mostly effective against circulating and metastasizing tumors; solid tumors are much less vulnerable to NK action against them. I failed pursuing your link so couldn't read the study, yet the premise that EPA inhibits NK is sound; EPA works  partly because it does keep lymphocytes from getting into tissue cells. Other very common factors that inhibit NK are fats, alcohol and steroids.

    EPA is showing itself to be useful against cancer; I seem to recall several types of neoplastic growths are less with EPA  supplementation. The EPA incorporated into a tissue cell's lipid membrane come into play through a series of steps; benefit is not as the EPA  molecule is being carried through the circulatory system.

  • woly

    4/15/2011 8:05:52 AM |

    Might-o'chondri-AL: can you please do us all a favour and start your own blog? I have started reading the comments section of many blog posts simply to see what you have written. All your posts are incredibly interesting, please keep up the good work!

  • Ensues

    4/15/2011 3:20:29 PM |

    Thanks for the info Frank.  I had indeed read up on niacin.  I started taking 500mg a couple months ago and then bumped to 1000mg after about a month.  I have not had a blood test yet to check the results.  I am hopeful though.  As for flush.  I have tolerated extremely well with really no problems except for one night.  After 2-3 months of no issues I experienced what I would call a crazy severe flush.  My skin was burning so bad I wanted to get it off.  Head to toe, hot and painful.  Not the "mild annoyance" I have read about.  It was nuts.  Lasted maybe an hour and a half.  Drank as much water as I could and a couple of aspirin.  Resumed 1000mg the very next day and have not had an issue since.  Very strange.  Thanks again for the comment.

  • Anonymous

    4/15/2011 4:44:01 PM |

    Be very careful when taking Niacin.  I can not tolerate even the small amount in a B-complex. My blood sugar increases, but even worse I become irrationally angry at the slightest provocation.

  • Anonymous

    4/15/2011 4:57:49 PM |

    Question regarding the reduction in NK cell activity ... could it pose a problem longterm?

    Would it possibly lead to a greater chance of infections (as some rodent studies have shown)?

    If someone had a metastasizing tumor, wouldn't fish oil then be contraindicated? I seem to recall DHA having some immune suppression activity too (not via NK however), but perhaps Vit E would counteract that.

    And then there is also that fish oil/rodent/colon cancer study:
    http://www.emaxhealth.com/1275/fish-oil-increases-risk-colitis-colon-cancer-mice

    Which seems to indicate DHA may be implicated negatively with colon cancer (in mice).

    And finally... I also recall the study testing oxidation values in people, using increasing doses of DHA (which is a bit of a messy way to test, but... whatever).

    http://www.futurepundit.com/archives/006499.html

    Somewhere between the 800mg and 1600mg levels of DHA, urinary isoprostane increased, which probably isn't such a good thing.

    I'm not anti-fish oil, as I take it myself. I am just wondering if too much (2-3+ g), may have some negative consequences longterm.

  • Might-o'chondri-AL

    4/15/2011 7:47:19 PM |

    Hi Anon,
    I have no suggestion on how to dose fish oil; I'd like to hear
    Doc's limitation on use for high
    trigs. This is for orientation on what you are discussing, as I understand things.

    Rodent and human models for chronic disease (inc. cancer) involve immune systems that are dissimilar; thus no cancer treatment has (to my knowledge) come from rodent results. That Michigan Univ. (2010) study fed mice that were geneticly pre-disposed to inflammatory bowels, in addition to fish oil, corn and safflower oils; those other oils can be converted into Arachidonic Acid, which is itself pro-inflammatory in some instances.

    Isprostanes in the urine are a bio-marker of oxidative activity; their existance is not automaticly evidence of damage to healthy cells. Some isoprostanes are also carried in an esterified form by our good old HDL.

    Isoprostanes come in several forms; they are mostly (but not exclusively) by-products of our natural anti-oxidants glutathione and glutathione peroxidase activity.  In other words when see isoprostanes in the urine it shows not only that the body had/has oxidative "stress", but that the body did something about it (ie: glutathione was busy doing it's job).

    DHA apparently works to increase the apoptosis (cell suicide/programmed death) of cancer cells, including bladder cancer. One of the theories explaining this effect is that fish oil integrates into the cancer cell lipid membrane; then it becomes part of a cascade of events that along the way produces levels of endo-peroxides
    (made inside the cell hydrogen peroxide).

    A threshold (ie: high enough
    dose)of fish oil must be reached to sustain a level of hydrogen peroxide that the cancer cell will take as a signal (ROS are internal cell signal molecules)
    to go into apoptosis. While all that hydrogen peroxide is being spun off, again and again, the cancer cell's innate anti-oxidant glutathione is trying to
    keep apace and neutralize it; so an endproduct (but not the endgame of the apoptosis dynamic that can "kill"
    developing cancer) is more isprostanes showing up in urine.

  • Renfrew

    4/16/2011 1:08:20 PM |

    When talking about dosage for fishoil what are we actually talking about?
    Milligrams per pill or mg for DHA/EPA.
    I am reading here 2-3 grams of DHA/EPA. So are we talking about the pure DHA/EPA content?
    1000 mg of fishoil is surely different from 1000 mg of DHA/EPA.

    Renfrew

  • Anonymous

    4/16/2011 5:30:28 PM |

    Renfrew: amounts of EPA/DHA.

    Total content of a fish oil capsule, which is typically 1g, is meaningless without concentration numbers.

    So when 3g is mentioned, it's 3g of EPA/DHA, not simply 3, one gram capsules. 3g of EPA/DHA could be up to ten capsules.

  • Renfrew

    4/17/2011 11:35:46 AM |

    Thanks for the clarification.
    How about minimizing the number of capsules in taking KRILL oil?
    Krill oil is a lot more bioavailable (phospholipids), compared to ordinary fish oil capsules. Less capsules for the same bioavailable amount of EPA/DHA.
    It also contains Astaxanthin which is good for brain, eye and prostate health.
    The ORAC test results in much higher anti-oxidant capacity.
    Why aren't we all taking krill oil??

  • Anonymous

    4/17/2011 5:40:37 PM |

    The reasons against krill oil:

    It's not cost-effective nor is it less capsules for an equivalent amount of EPA/DHA (in fact, it's many more).

    I know of one comparison study which did show krill oil being about 50% or so more bioavailable that fish oil. But krill oil is like 5-10x the price of fish oil (based on EPA/DHA dosing). So one can do the math there.

    And there is also the fact that krill oil has been much less studied than fish oil has.

    Astaxanthin is interesting and one day I'd love to see Dr. Davis touch upon it on this blog, state if any of his patients use it, etc. But if you want astaxanthin, I'd think it'd make more sense and be a lot cheaper just to buy astaxanthin (from algae). I've seen it going for as low as $8 for 120, 4mg caps and even non-sale prices are like $10/60 caps. Much cheaper than krill oil.

  • reikime

    4/18/2011 4:27:51 AM |

    I have considered krill oil as i am very intolerant of anchovies and most fish oil caps contain it.

    Tried the Salmon oil, but ewww...nasty!

    Need the benefits of fish oil, but not the side effects.

    Thoughts? Time to take the Krill?

  • Anonymous

    4/18/2011 9:35:23 AM |

    Hey Dr Davis

    Have a look at Gary Taubes' latest post with blood lipid test results:

    http://www.garytaubes.com/2011/04/before-sugar-were-talking-about-cholesterol/

    Nina

  • Caveman

    4/30/2011 1:12:18 AM |

    Any reason to be concerned with very low trigs? Below are my latest blood test results and the trigs seem to be very low. Does this indicate anything?


    Glucose = 68.4 mg/dl
    HDL = 59 mg/dl
    LDL = 98 mg/dl
    Triglycerides = 17 mg/dl

  • James

    5/23/2011 4:24:46 PM |

    A little confused
    Before I had my latest blood test I thought having low trigs and a good TC/H ratio was the best indicators of CVD. Thanks to Dr. Davis I discovered the NMR LipoProfile and Vitamin D tests and  added them to my panel.

    The good part:
    Trigs: 50
    Total Chol: 198
    HDL-C: 70
    LDL-C: 118 (slightly elevated)

    That gives me a TC/H of 2.8, which I assume is excellent.

    But now, the surprising not so good news:
    LDL-P: 1410 (High)
    Small LDL-P: 613  (High)
    Vit D: 31.4 (Low)

    So, how can I have trigs below 60 and have a high LDL particle number and 43% of them small LDL-P?

    Can anyone help me interpret these results? BTW, I am  a 50 yo man in good shape and weight.

    Thanks in advance

  • Alfredo

    6/2/2011 3:57:56 PM |

    Hi, Dr. , please check your email system, I have not been recieving my emails since you moved to this new site.

    THanks

  • Bill

    6/10/2011 8:48:01 PM |

    The text
    "1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

    2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

    3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

    4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack."
    does not appear to be sourced from the sole referenced article in this blog post. The referenced article (Austin et al, 1990) is examining a specific human genetic phenotype in regards to triglyceride, HDL and LDL levels. Is there another source of this information, or are there specific page(s) I can read of the article to derive the same information?

  • Paul Lee

    7/6/2011 12:47:01 PM |

    Just got back from the docs and have mixed feelings as she prescribed a daily statin! However reading up on the low carb sites and on this blog it might not be all bad news! Fasting Triglycerides were 1.1 (96) and TC was 7.1 (6.22) I'm in the UK and hope I hope I've converted properly. I eat low carb, avoid cereals and am reasonably active, in addition to intermittently fasting. I think I've lost weight, that was one of the reasons I went to see the doctor as I thought my weight loss had stalled, but my BMI was down to 23 from 25/6. Its slow but getting there but I did read on some of LC forums that Triglycerides might be elevated whilst actively loosing weight. Clearly there is more work to do and I'm tempted to get a second test. I won't be taken a statin even though its free (provided on the NHS).

  • Rickey

    10/20/2011 5:47:51 AM |

    I know very little about Krill Oil. There had been a bunch of posts regarding Krill oil Brand on the various forums and blogs. After doing all research on internet, i came across with Krill oil Professional, this brand product is awesome. I ordered it online from there website at very competitive pricing. And now iam feeling very much relaxed from my Arthritis joint pain/stiffness relief.

Add comment

Loading

Add Boston Globe to the list of heart scan blunders

17. September 2008 William Davis (15)
Yet another piece of mass media misinformation hit the airwaves today. This time it's not from the New York Times or the LA Times, both of which have previously mangled the issues surrounding heart scans. This time it's from the Boston Globe.

In an article titled What is a calcium scan for heart disease, and who should undergo the test?, the report states:

". . . calcium scans may not be a good idea, or prove terribly useful, for most people. For one thing, the scans expose a patient to significant radiation - equivalent to roughly 50 chest X-rays" said Dr. Warren Manning, chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center."

As many before him, Dr. Manning is confusing two tests: CT coronary angiography and CT heart scanning. Perhaps we can't blame him: This technology has had its weakest following in the northeast, for reasons not entirely clear to me. (In fact, Track Your Plaque followers have had the greatest struggle obtaining heart scans in that part of the country.) Nonetheless, you'd think he'd have his simple facts straight before talking to the press. Unfortunately, hospital public relations departments will usually just grab whoever they can willing to talk to the press--regardless of their expertise or lack of.


The story goes on to say:

. . ." it's not clear what to do with the results from a calcium scan. If you have diabetes, high cholesterol, high blood pressure, or a family history of heart disease, you already know - or should know - that you are at increased risk of heart problems and should lower these risk factors. So, a calcium scan provides little additional information," Manning said.

"Moreover, even a high score doesn't necessarily mean that the calcified plaque in your arteries is obstructing blood flow, said Dr. Adolph Hutter, a cardiologist at Massachusetts General Hospital."

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death," said Manning.

And if you get a low calcium score, a sign of little or no calcification of plaques, that's not very useful, either, because it could be wrong, or it could be right but lull you into believing you do not have to exercise and watch your diet, cholesterol, and blood pressure levels. "You can still be at risk even if your calcium test is negative," Hutter said.


It is truly shocking how little many (not all, thank goodness) of my colleagues really know about 1) heart scans, 2) coronary disease prevention, and 3) prevention in general. These same "experts" likely advocate high-dose statin drugs and low-fat diets for people at risk. They likely refer patients to the American Heart Association for diet advice and themselves obtain a lot of information from the pharmaceutical industry. The notion of identification, tracking, and purposeful reversal of coronary plaque is entirely foreign to this bunch.

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death." Well, take a look at a graph from a database of 25,000 people undergoing heart scans then observed for several years afterwards:




You can see quite clearly from the curves that heart scan scores very clearly predict your future (if no preventive action is taken). The higher the score, the greater the likelihood of heart attack and death. How much clearer can it get?

The most recent addition to this literature is the PREDICT study which concluded:

Hazard ratios relative to CACS [coronary artery calcium scores] in the range 0-10 Agatston units (AU) were: CACS 11-100 AU, 5.4 (P = 0.02); 101-400 AU 10.5 (P = 0.001); 401-1000 AU, 11.9 (P = 0.001), and >1000 AU, 19.8 (P < 0.001).

In other words, a heart scan score of >1000 is associated with a 20-fold increased risk of cardiovascular events (without preventive efforts). That kind of predictive power and quantitative confidence simply cannot be squeezed out of blood pressure and cholesterol values.

How about the 2008 University of California-Irvine study from the New England Journal of Medicine (do the northeast docs even pay attention to something that is published in their own neighborhood?) that reported:

There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%.

How about the Prospective Army Coronary Calcium (PACC) project (men average age 43 years):

"In these men, coronary calcium was associated with an 11.8-fold increased risk for incident coronary heart disease (CHD) (p = 0.002) in a Cox model controlling for the Framingham risk score. Among those with coronary artery calcification, the risk of coronary events increased incrementally across tertiles of coronary calcium severity (hazard ratio 4.3 per tertile)."

Calcium score provided additional information even after factoring in the Framingham risk score.

That's just a sample of the studies. There are a number more.

Add to these conversations the fact that, unlike reducing blood pressure or LDL cholesterol, the heart scan score is a quantification of the disease itself. It can also be tracked over time to gauge the success or failure of prevention efforts. To believe that blood pressure reduction or LDL cholesterol reduction is sufficient to eliminate risk is something only a fool would believe.



Contary to the above statements, the data are clear:

--The higher the heart scan score, the greater the risk. This has been demonstrated beyond any shadow of a doubt in at least a dozen published studies. In fact, heart scan scores outshine lipid/cholesterol values several-fold.

--A person with a zero score has a nearly zero risk for cardiovascular events over a 5-year timeline.

--Heart scans are the only quantitative test available of coronary atherosclerotic plaque. This means that they can be repeated to gauge progression or regression. Cholesterol does not do that. Stress tests do not do that.

--Heart scans are not the same as CT coronary angiography.

--The lack of "need" for a procedure does not equate to the absence of disease.

The power of heart scans is that they can uncover evidence for coronary atherosclerotic plaque 10 years before a cardiac disaster strikes. Witness Tim Russert's heart scan score of 210 in 1998 at age 48. 10 years later, you know what happened.

Beware the camipaign of misinformation and ignorance that continues that is hell-bent on maintaining the procedural status quo or locking us into a "drugs for all" mentality.

What's worse than sugar?

16. September 2008 William Davis (11)
There are a number of ways to view the blood sugar-raising or insulin-provoking effect of foods.

One way is glycemic index (GI), simply a measure of how high blood sugar is raised by a standard quantity of a food compared to table sugar. Another is glycemic load (GL), a combination (multiplied) of glycemic index and carbohydrate content per serving.

Table sugar has a GI of 65, a GL of 65.

Obviously, table sugar is not good for you. The content of white table sugar in the American diet has exploded over the last 100 years, totaling over 150 lb per year for the average person. (Humans are not meant to consume any.)

What is the GI of Rice Krispies cereal, organic or not? GI = 82-- higher than table sugar. GL is 72, also higher than table sugar.

How about Corn Flakes? GI 81, GL 70--also both higher than sugar.

How about those rice cakes that many dieters will use to quell hunger? GI 78, GL 64.

How about Shredded Wheat cereal? GI 75, GL 62.

All of the above foods with GI's and GL's that match or exceed that of table sugar are made of wheat and cornstarch. Some, like Shredded Wheat cereal and rice cakes, don't even have any added sugar.

Stay clear of these foods if you have low HDL, high triglycerides, high blood sugar, or small LDL. Or, for that matter, if you are human.

Keep the eloquent words of New York University nutritionist, Marion Nestle, author of the book, Food Politics, in mind:

“Food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.” ??

Are sterols the new trans fat?

13. September 2008 William Davis (16)
By now, I'm sure you're well-acquainted with the hydrogenated, trans fat issue.

Hydrogenation of polyunsaturated oils was a popular practice (and still is) since the 1960s, as food manufacturers sought a substitute for saturated fat. Bubbling high-pressure hydrogen through oils like cottonseed, soybean, and corn generates trans fatty acids. These man-made fatty acids, while safe in initial safety testing, proved to be among the biggest nutritional mistakes of the 20th century.

Trans fatty acids have been associated with increased LDL cholesterol, reduction in HDL, oxidative reactions, abnormal rigidity when incorporated into cell membranes, and cancer. Trans fats still dominate many processed foods like chips, cookies, non-dairy creamers, food mixes, and thousands of others. They're also found prominently in fast foods.

Fast forward to today, and most Americans have become aware of the dangers of trans fats and many try to avoid them.

But I worry there is yet another substance that has worked its way into the American processed food cornucopia that has some potential for repeating the trans fat debacle: sterol esters.


Sterols are naturally-occurring oils found in vegetables, nuts, and numerous other foods in small quantities. Most of us take in 200-400 milligrams per day just by eating plant-sourced foods.

Curiously, the chemical structure of sterols are very similar to human cholesterol (differing at one carbon atom). Sterols, by not fully understood means, block the intestinal absorption of cholesterol. Thus, sterol esters, as well as the similar stanol esters, have been used to reduce blood levels of total and LDL cholesterol.

So far, so good.

The initial commercial products, released in the late 1990s, were Take Control (sterol) and Benecol (stanol), both of which were marketed to reduce cholesterol when 2-3 tbsp are used daily, providing 3400 – 5100 mg of sterol or stanol esters, about 10- to 20-fold more than we normally obtain from foods. Several clinical trials have conclusively confirmed that these products reduce cholesterol levels.

They do indeed perform as advertised. Add either product to your daily diet and LDL cholesterol is reduced by about 10-15%. In fact, in the original Track Your Plaque book, these products were advocated as a supplemental means of reducing LDL when other methods fell short.

In 2008, there are now hundreds of products that have additional quantities of sterol esters in them, such as orange juice, mayonnaise, yogurt, breakfast cereals, even nutritional supplements. Most of these products proudly bear claims like "heart healthy." Stanol esters have not enjoyed the same widespread application. (I believe there may be patent issues or other considerations. However, it's the sterols that are the principal topic here, not stanols.)

Now, here's where it gets a bit tricky. There is a rare (1 per million) disease called sitosterolemia, a genetic disorder that permits the afflicted to absorb more than the usual quantity of sterols from the intestine. While you and I obtain some amount of sterols from plant-based foods, absorption is poor, and we absorb <10% of sterols ingested. However, people with sitosterolemia absorb sterols far more efficiently, resulting in high blood levels of sterols that result in coronary disease and aortic valve disease, with heart attacks occurring as young as late teens or 20s. Treatment to block sterol absorption are used to treat these people.

There are also a larger number, though still uncommon (1/500) of people who have only one of the two genes that young people with sitosterolemia have. These people may have an intermediate capacity for sterol absorption.

Okay, so what does this have to do with you? Well, if you and I now take in 10-20 times greater amounts of sterol esters, do our blood levels of sterols increase?

Several studies now suggest that, yes, sterol blood levels increase with sterol ingestion. One study from Finland, the STRIP Study, showed that children who had double usual sterol intake increased blood levels by around 50%.

Similarly, a Johns Hopkins study in adults with only one of the genes ("heterozygotes") for sitosterolemia increased sterol blood levels by between 54-116% by ingesting 2200 mg of sterols added per day, despite reduction of LDL cholesterol levels.

Even people with neither gene for sitosterol hyperabsorption can increase their blood levels of sterols. But the crucial question: Do the blood levels of sterols that occur in unaffected people or in heterozygotes increase the risk of coronary heart disease? The answer is not known.

Despite the several clinical trials performed with sterol esters, all of them have examined LDL and total cholesterol reduction as endpoints, not cardiovascular events. It is conceivable that, while sterol esters reduce cholesterol, risk for heart disease is increased due to higher blood levels of sterols.

The question is not settled. For now, it is just a suspicion. But that's enough for me to steer clear of processed foods supplemented with these uncertain sterol esters. My previous recommendations for sterol ester products will be removed with the next edition of Track Your Plaque. Until we have solid evidence that there are no adverse cardiovascular effects of sterol esters, in my view they should not be part of anyone's heart-disease prevention program.

(The same argument does not seem to apply to stanol esters, such as that contained in butter-substitute Benecol, since stanol esters are not absorbed at all and remain confined to the intestine.)

The Diabetes Gold Rush

11. September 2008 William Davis (9)
Lou came into the office. Clearly, his program had gone sour.

Lou had initially obtained wonderful control over his heart scan score of 1114, having reversed modestly in his first three years of effort through correction of his multiple causes (including low HDL, severe small LDL, Lp(a), and a diabetic tendency).

But Lou now came into the office red-faced and sporting a big bulging abdomen. Blood sugar? Now in the overtly diabetic range. Lou said that his primary care doctor had suggested that he start on three new medications (glucophage, injectable Byetta, and Actos) to control his blood sugar. His doctor also told him to increase his intake of fibers by eating more "healthy" breakfast cereals like Cheerios.

Lou had apparently done just that (added "healthy" fiber-rich foods) even before his doctor had suggested it. (Lou failed to remember the several conversations we'd had about healthy eating.) Unfortunately, Lou also failed to connect his increased intake of "healthy fiber-rich foods" and his growing abdominal girth (his "wheat belly").

Here's the dirty little secret: Much of the world wants you to be diabetic. It is the health gold rush of this century. "Go West, young man!"




To find out what I mean, you need only ask: Who profits when people become diabetic? That's easy:

The pharmaceutical industry--Diabetes is a booming growth industry, a source of tens of billions of dollars of revenue, poised for enormous growth as the population ages and gets fatter. It is common for a newly-diagnosed diabetic to be given new prescriptions for two or three drugs with a monthly cost of $300. Of course, the chronic nature of the disease make this far more profitable than, say, a two week course of antibiotics. Presently, 70 new drugs are under development.

Diabetes drug maker Novo Nordisk reported a 25% increase in revenues in 2007 from diabetic agents in the North American market, along with near $2 billion increase in profit for the year. Merck's recently-released DPP-4 inhibitor, Januvia, has already sold $668 million in 2007 and is growing rapidly.

The medical device and supply industry. Take a look at the Medtronic quarterly earnings report, detailing the breakdown of their record-setting quarterly revenue of $3.7 billion:

Diabetes revenue of $269 million grew 12 percent driven by sales
of consumables, the accessories required by insulin pump users, and
continuous glucose monitoring products. Revenue from international
sales grew 31 percent over the same quarter last year.

That's what I call a growth industry.

The processed food industry. The food industry is as big or bigger than the drug industry. ADM, Kraft, General Mills all have annual revenues in the $12-50 billion range. There are plenty of others.

When we're told, for instance, that Cheerios reduces cholesterol, we're not told that it skyrockets blood sugar or triggers small LDL. When we're sold whole wheat crackers, Cocoa Puffs (which the American Heart Asscociation says is heart-healthy), or granola bars, hunger is stimulated, impulse to eat more grows, blood sugar escalates, we get fat, we get diabetic. It's a simple formula.

So be aware that there is little incentive among corporate giants in the food, medical device, or drug industries to encourage behaviors that decrease the incidence of diabetes. In fact, there is enormous financial incentive to make sure that diabetes continues to grow at the startling rate it has over the last decade.

To be sure, the drug and medical device industry will also develop better tools to deal with diabetes and its complications. But the very best way to deal with diabetes is to not develop it in the first place.

What else is there?

7. September 2008 William Davis (11)
This question comes up frequently:

Aren't there any alternatives to heart scans performed on a CT or EBT device?

Yes, there are.

First of all, heart scans are performed best on an electron-beam CT device (EBT) or a 64-slice multi-detector CT (MDCT) device. (While they are also obtainable through less-than-64 slice CT devices (e.g., 16 slices and less), I would advise against it because of the excessive radiation exposure and poor accuracy.) CT heart scans are not to be confused with now more popular CT coronary angiograms, which are performed on the same devices but require intravenous x-ray dye and many times more radiation.(See CT scans and radiation exposure and Heart scan frustration.) Heart scans currently form the basis for the Track Your Plaque program, a program of tracking plaque in the hopes of stopping or reversing the otherwise inevitable 30% per year increase.

Let's confine our discussion to people without symptoms, meaning people like you and me sitting at home, not in an emergency room having chest pain or other similar acute symptomatic presentation.

Among the other ways to uncover hidden coronary plaque:

--Heart catheterization--to yield a coronary angiogram. Yes, this does tell us whether coronary plaque is present. However, it is invasive, expensive, and crude. (I've performed 5000 over my career; they are crude, though useful, tools in acute settings like unstable symptoms or heart attack, a different situation.) Coronary angiography is also non-quantitative. While they provide a value like "40% blockage mid-way in right coronary" or "90% blockage in left anterior descending" they do not provide a trackable lengthwise index of total plaque volume. Identifying severe blockages in people with symptoms leads to stents, bypass surgery and the like, but it is not practical nor of long-term usefulness in apparently, healthy people without symptoms.

--Carotid ultrasound--Here's is where a lot of confusion comes from. Standard carotid ultrasound (U/S) performed in virtually every hospital and many clinics will yield crude qualitative results, e.g., "16-49% stenosis (blockage) in right internal carotid artery". The crude value range is because much of carotid U/S is based on flow velocities, not just direct visualization of the plaque itself ("2-D imaging). However, if carotid stenosis of any degree is identified, the likelihood of silent coronary plaque is much greater.

Limitations: The qualitative, non-quantitative nature of carotid U/S make it difficult to follow long-term in a precise way. Also, this is carotid plaque, not coronary plaque. It makes it very difficult to follow carotid plaque as an indirect means of tracking coronary plaque. The two arterial territories, carotid and coronary, do not track together: there are divergences in many people, with carotid plaque absent in some people with advanced coronary plaque, carotid plaque more susceptible to different risk factors than coronary. So carotid U/S is helpful for its own purposes, but not terribly helpful for coronary tracking.

How about carotid intimal-medial thickness (CIMT) obtained also with carotid U/S? CIMT is a useful index of bodywide atherosclerosis. CIMT is simply a measure not of plaque (and is measured in regions of the carotid artery away from plaque), but of the thickness of the lining of the carotid arteries. Everybody has a measurable CIMT, but it thickens as atherosclerosis grows. CIMT is a radiation-free test that takes several minutes.

Limitations: Hardly anybody does it outside of research protocols. I know of no hospital or clinic in my area that performs CIMT, though it is slowly being adopted in some centers. It is also difficult to rely on repeated tests, because there is substantial variation when one technologist or another performs it. CIMT is also a flawed index of coronary plaque. When CIMT is compared to heart scan scores, CT coronary angiography, or conventional coronary angiography, CIMT correlates about 60-70% with the degree of coronary atherosclerosis.

CIMT is therefore a useful test for research, but a distant 2nd choice--if you can obtain it.

--Ankle-brachial index (ABI)--ABI is a crude measure, simply a comparison of the blood pressure (obtained with a blood pressure cuff) in the legs divided by blood pressure in the arms. The ratio is called ABI. Any ABI <1.0, meaning less pressure in the legs compared to the arms, is indirectly indicative of advanced coronary disease. ABI is, in fact, a very powerful predictor of cardiovascular events. If ABI is <1.0, your future risk for heart attack is very high, even in the absence of symptoms.

Limitations: The vast majority of people with heart disease, even those having undergone stents or bypass surgery, have normal ABI's. Virtually all people with high heart scan scores have normal ABI's. In other words, ABI is a measure of very advanced atherosclerosis only.

--Stress tests--I lump all stress tests together in their various forms, e.g., stress thallium, stress Cardiolite, stress Myoview, persantine/adenosine Cardiolite, dobutamine echocardiography, etc. Stress tests are tests of coronary blood flow, not of plaque. Stress tests are useful in people with symptoms, like chest pain or breathlessness, since stress tests are provocative tests that can help determine whether reduced coronary blood flow is the cause behind a symptom, or whether hiatal hernia, esophagitis, gallstones, pleurisy, musculoskeletal causes, or some other process is behind symptoms.

Limitations: Stress test are virtually useless in people without symptoms. This is why people like Tim Russert and Bill Clinton, both without symptoms, underwent several (Russert 3, Clinton 5) nuclear stress tests---all normal. You know what happened to them. Stress tests do not reliably uncover hidden coronary plaque in people without symptoms. Stress tests are, like coronary angiograms, non-quantitative. They are normal or abnormal.


Outside of experimental settings, that's it.

You can probably see why I advocate CT heart scans for tracking plaque. I do not advocate heart scans because I sell them (I don't), because scan centers pay me to say these things (they don't, and in fact my relationship with my usual heart scan centers has become deeply contentious, though I still endorse the technology). I say that heart scans are superior because they are, in 2008, the only way to 1) identify and 2) track coronary plaque that is easy, safe, low-radiation, and reasonably priced (<$200 in Milwaukee at 5 centers).

The need for a technology that allows tracking of plaque, not just initial identification, is also an important distinction. People who've had some measure of atherosclerosis all catch on to this eventually. "Can I reverse it?" is an inevitable question once the disease is identified in some way. So a tool for tracking over time to gauge the success or failure of a program of prevention can be assessed.

Perhaps in 10 years, another technology will emerge as the preferred means to do the same, but better. If that proves true, we will convert to that technology. But today heart scans performed on CT heart scans are the only rational way to both detect, then track, coronary atherosclerotic plaque.

Let's gamble with your health

5. September 2008 William Davis (4)
Let's play a game.

I'm going to list some lipid patterns and you tell me whether or not the person with these values has heart disease.

Patient 1

Total cholesterol 150 mg/dl
LDL cholesterol 75 mg/dl
HDL 50 mg/dl
Triglycerides 125 mg/dl


Patient 2

Total cholesterol 300 mg/dl
LDL cholesterol 200 mg/dl
HDL cholesterol 35 mg/dl
Triglycerides 325


Patient 3

Total cholesterol 300 mg/dl
LDL cholesterol 100 mg/dl
HDL cholesterol 25 mg/dl
Triglycerides 875 mg/dl



Let's say that any one of these profiles is yours. Should you be getting your affairs in order, preparing for your cardiac catastrophe? Should you demand a stress test from your doctor, hoping that it will shed some light on your dilemma? Should you go ahead and go to the all-you-can-eat rib restaurant, content that you will be attending your granddaughger's wedding in 2020 in full health?

If you can tell, you're a lot better at this than I am.

I provide consultation to other physicians and patients on complex hyperlipidemias in my area. In other words, if someone has a difficulty to manage lipid disorder, the doctor sends the patient to me.

Managing these wildly variable values is the easy part. Deciding whether or not heart disease is concealed within the patient . . . well, that's the hard part.

Let's take it a step further: Suppose all three profiles also have 50% of all LDL particles as the abnormal small particles. And they all have a lipoprotein(a) level of 50 mg/dl, an abnormally high level.

How about now: Can you tell whether any or all of these people have hidden heart disease?

What if they are 20 years old? Does that make a difference?

What if they are all females over 65 years--how about now?

If the only tool you have to divine the presence of hidden heart disease is a lipid panel, or even a lipoprotein panel, then the best you can manage is to hazard a guess based on statistical probability. You also assume that this "snapshot" represents the sorts of values someone has had for their entire lives. You cannot factor in the fact that the first person gained 60 lbs in the last three years since completing menopause. You can't factor in that patient 2 smoked two packs of cigarettes a day for 25 years, but quit 10 years ago.

It's also foolhardy to believe that every known cause of heart disease is currently identifiable and revealed by modern-day blood testing.

A heart scan is simply a means to quantify the sum-total of risk factors--causes--that have exerted an effect up until the moment of your scan. It will reveal the quantity of coronary atherosclerotic plaque present, regardless of whether you stopped smoking 20 years ago or lost 30 lbs last year.

For these reasons, nothing can replace the value of quantifying plaque: not cholesterol, not the Framingham risk calculation, not measures of small LDL or lipoprotein(a), not the presence or absence of symptoms. In 2008, the method of choice for measuring plaque remains a CT heart scan. Perhaps in 10 years it will be some other method.

As always, let me remind Heart Scan Blog viewers that I make this point NOT to sell heart scans, which I have no reason whatsoever to do. I say this because we require a tool to track this potentially fatal disease. We require a yardstick for tracking progression or regression. The only tool that suits these purposes in 2008 is a CT heart scan.

Who knows what

4. September 2008 William Davis (4)
You know that cynical old saying:


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

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

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

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

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


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


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

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

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

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

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

But they are coming.

“Too many false positives”

4. September 2008 William Davis (6)
“Do you really think I need a heart scan?” asked Terry.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Triglycerides divided by five

3. September 2008 William Davis (8)
Here's a bit of lipid tedium that might nonetheless help you one day decipher the meaning of shifts in your cholesterol panel.

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

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

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

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

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

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

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


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

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


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

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

Nonsense, absolute nonsense.

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

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

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

Who reads The Heart Scan Blog?

2. September 2008 William Davis (0)
In the Heart Scan Blog, I am often guilty of speaking out loud of my varied thoughts on this crazy thing that we've created called the cardiovascular healthcare machine. But I discuss it in the context of asking "How could this be done better--better outcomes, more patient-friendly, more accessible . . . more do-it-yourself?

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

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

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

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

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