Cureality | Real People Seeking Real Cures

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.

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.

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.

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.

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.

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.

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:

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.

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, 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 is C-reactive protein (CRP)?

It is a blood-borne protein that originates in the liver and serves as an index of the body's inflammatory state. It is triggered by yet another inflammatory signal molecule, interleukin-6.

What triggers this cascade of inflammatory markers? Any inflammatory stimulus, such as being overweight, lack of exercise, vitamin D deficiency, viral illness no matter how trivial, any inflammatory disease like arthritis, small LDL, high triglycerides, poor diet rich in processed foods, resistance to insulin, any injury, incipient diabetes, hidden cancer, lack of education (no kidding), etc.

In other words, many, many conditions, from trivial to serious, trigger increased inflammatory markers like CRP.

A recent analysis (Genetically elevated C-reactive protein and ischemic vascular disease of persons with genetically elevated levels of CRP) suggests that CRP does not, by itself, cause atherosclerotic disease. CRP is therefore simply a marker for conditions that heighten inflammatory responses.

The AstraZeneca people sponsored the enormous JUPITER study of the statin drug, Crestor, that has been causing a stir, mostly glowing pronouncements of how the world would be a better place if everyone took Crestor.

In JUPITER, nealry 18,000 people (men 50 years and over, women 60 years and over) took 20 mg per day Crestor for two years. Participants all had starting LDL cholesterols in the "normal" range of no higher than 130 mg/dl and elevated CRP of 2 mg/dl or greater.

Crestor treatment resulted in 44% reduction in nonfatal heart attack, nonfatal stroke, hospitalization for unstable angina, revascularization (bypass surgery, stents) and death from cardiovascular causes. The reduction in nonfatal heart attack was most marked at 55%.

Admittedly, these are impressive results. Benefits held true for both males and females. At the very least, JUPITER should put to rest some of the fringe arguments that statins do not reduce cardiovascular events. They do. There is no sense in arguing against that. While we might argue about the value of statins in various subsets of people, there is no doubt that they do indeed exert a significant effect.

However, contrary to the hype and broad pronouncements of my c All posts by william-davis

Wheat-free and still fat

15. February 2008 William Davis (14)

Readers of The Heart Scan Blog know that I preach a diet that contains foods with low glycemic index to control weight, raise HDL, and reduce triglycerides, blood sugar, and small LDL.

A crucial aspect of a low glycemic index approach is to sharply reduce, preferably eliminate, wheat products.

I pick on wheat specifically because it has come to dominate the American diet. Look at the shelves in the supermarket: aisle after aisle of processed wheat products. The bread shelves alone in some of the grocery stores in my neighborhood are 40 feet long, six shelves high. There's also breakfast cereals, granola products, cookies, cakes, baking products, pretzels, crackers, pasta, and on and on.

Wheat products like these are tasty and they're addicting--literally. Test animals given processed wheat will eat more and gain more weight. Wheat fails to trigger satiety. So laboratory mice--and you and I--eat and eat, because eating wheat stimulates appetite, creates a hunger for more wheat, and a vicious cycle ensues. Eliminating wheat, on the other hand, results in dramatic drop in appetite, substantial weight loss, followed by correction of the metabolic disruptions it created.

A quick Google search for "gluten-free" turns up a startling array of wheat-free, gluten-free, yet high glycemic index products. The breakfast cereal pictured, for instance, can do as much damage as most wheat containing products--though it won't cause gluten enteropathy (also known as "celiac disease").

The product shown contains:

Brown rice flakes, rice bran, evaporated cane juice, brown rice syrup, raisins, cinnamon, gum arabic, vanilla, molasses, ground flaxseed, rosemary extract.

A 1/2-cup serving contains:
Total Carbohydrate 31g
Dietary Fiber 5g
Sugars 8g

And I'll bet that most people eat a lot more than a half-cup serving.

But you and I are not laboratory mice. If deprived of wheat, many people will then seek out processed rice products (rice cakes, Rice Krispies), processed cornstarch or cornmeal products (tacos, cornbread, many processed foods using these products for texture or thickness), or other products labeled "gluten-free."

Going wheat-free for our purposes is not about avoiding the gluten in wheat. It is about seizing control of appetite, eliminating a food that disrupts insulin responses, reduces HDL, raises triglycerides, and creates small LDL particles. But this applies to processed corn, rice, and other high glycemic index foods, as well.

So, occasionally, someone will declare, "I've eliminated wheat! Now I only eat rice, corn, and I've discovered all the gluten-free alternatives!"

Unfortunately, they've traded one evil for another. So it's not just about wheat. It's really about reducing or minimizing foods that mess up metabolic responses and lead to coronary plaque growth. Wheat is the biggest culprit and so I focus on it. However, you could easily transfer far less popular rice and corn products into center stage and allow them to wreak all the health damage of wheat.

Going wheat-free for our atherosclerotic plaque-control purposes is not the same as going gluten-free. So be careful of the distinction.

Wheat-free gummi bears:

Contents:
Organic dehydrated cane juice, organic corn malt syrup, organic juice concentrates (may contain organic apple, organic apricot, organic aronia, organic carrot, organic cranberry, organic elderberry, organic lemon or organic red beet), organic spinach powder, organic apple pectin, citric acid, natural fruit flavors.

Virtually pure sugar--yet wheat-free.

Wheat-free rice bread

Ingredients:
White rice flour, water, honey, soy oil, natural gum, salt, yeast, natural gum

Copyright 2008 William Davis, MD

Heart disease is reversible

13. February 2008 William Davis (10)

In a previous post, Take this survey: I double-dare you, I posed a challenge:

Ask your doctor: Is heart disease reversible? Their answer:

1) No. Heart disease is definitely not reversible.

2) Yes, in rare instances, like lightning striking twice.

3) Yes, of course it is! Let's talk about how to do it!

I predicted that few readers of this blog would respond. I also predicted that the few who did would respond with the first answer, Heart disease is definitely not reversible. After all, in nearly all medical practices, the only parameters routinely followed to track risk for heart disease are LDL cholesterol and blood pressure. A measure of the disease itself (i.e., coronary atherosclerotic plaque) is not followed. So how can your doctor actually tell whether heart disease is reversed or not? When I engage in this conversation with colleagues, it goes no farther than rolled eyes or a snort. In my experience, talking about reversal of heart disease is a wasted effort.

To my great surprise, this simple survey received a total of 177 responses. Even more surprising, 122 (69%) of respondents chose number 3, claiming that their doctor said that heart disease is reversible.

Overall results:

1--31 responses (17.5%)

2--24 responses (13.5%)

3--122 responses (69%)

Now wait a minute: Where is the disconnect? Why are doctors saying that heart disease is reversible, yet not following this concept in practice? Contrary to the survey results, I have yet to meet a patient who said their doctor was trying to reverse their heart disease. Of course, this may be a skewed population, but I find it hard to believe that the prevailing view is that heart disease is reversible.

Anyway, this simple survey cannot settle the why or how, nor can it suggest just how prevalent this opinion is.

I am encouraged by these results. If true, it means that the message that heart disease is a reversible process is spreading. It may be make-believe heart disease reversal as preached by Dr. Dean Ornish or claimed by statin drug manufacturers. It may be the hocus-pocus of practices like chelation, or scams like nattokinase. But perhaps the seed of this notion has been planted in the minds of the medical community.

I'd be interested in hearing from the respondents who reported that their doctor said heart disease is reversible. How exactly are they going about achieving reversal?

Looking for health in all the wrong places

12. February 2008 William Davis (11)

The American public now has unprecedented freedom to explore new directions in health.

Never before have we had the enormous resources now available to add to our health experience: nutritional supplements, endless books on health and diet, the internet, online discussion groups, insurance products to permit spending on self-directed health services like medical savings accounts and flex-spending. The Track Your Plaque program is just one facet of this emerging and exciting area of self-empowerment in health. Compare what you can achieve with such a program with the situation of just 25 years ago, when the most you might get to reduce your risk for heart disease was to take the (largely ineffective) drug cholestyramine, probucol, and a low-cholesterol, low-fat diet.

Unfortunately, it also means that people have unrestrained potential to be tripped up, to be misled down some dead end of health that fails to accomplish desired goals, maybe even dangerous. The more freedom we have, the greater the choices, the more room we have to screw up.

Among the unproductive strategies I've witnessed recently:

--Nattokinase--The staying power of this scam continues to shock me. There is no rational basis for its use. A woman today declared that she would like to stop the warfarin that she was taking to prevent stroke from atrial fibrillation by taking nattokinase. This would be a mistake that could cost her a major and disabling, even fatal, stroke. Though warfarin is far from perfect, it at least achieves its goal of reducing stroke risk. Nattokinase does not. Nattokinase does nothing but make money for the people who sell it.

--Poly-nutritional supplements. You've heard of polypharmacy, the phenomenon of taking numerous medications with overlapping effects and side-effects, usually because of multiple doctors, each prescribing drugs without knowledge or interest in what colleagues are prescribing. I'm seeing the same phenomenon with supplements: 20,30, or more supplements per day, all in the hopes of heightening health. A focused few supplements is, in my view, superior to a shotgun approach of trying to improve health by taking hawthorne, silymarin, chrysin, calcium, Chinese herbs, and 25 other supplements.

--Chelation--Based on the notion that heavy metal toxicity causes heart disease; removal of heavy metals cures it. I've read some of the books on chelation, in addition to the slim scientific data, to decide whether there was anything to it. In my view, it is a complete and utter scam. It does make money for its practitioners, however. That's not to say that heavy-metal chelation doesn't have a role in health--it does. But it serves no purpose in coronary disease prevention and control.

--Colonic purges--Achieved by a number of routes, some oral, others via enema. Promotions for purging are often accompanied by a pile of scum that apparently lined somebody's intestinal tract. Purges purportedly, well, purge it from the intestine. This is also plain nonsense. There is no such toxic scum lining anybody's intestinal tract. However, if calorie restriction or a fast results inadvertently from the effort, perhaps some good comes from it.

--Statin drug alternatives--The unprecedented $27 billion dollar a year success of the statin drug industry, accompanied by the enormous marketing push by their manufacturers, has spawned an entire industry of statin alternatives. They range from red yeast rice, to guggulipid, to various concoctions of sterol esters, Chinese herbs, chitosan, and a variety of others. Some actually do reduce cholesterol a few points. Preparations like red yeast rice even pose a side-effect profile not too different from the prescription statin agents. Unfortunately, even among those agents that work, the effects tend to be small to trivial. While I am no lover of statin drugs nor the statin drug industry, I find these preparations to be anemic imitators. You'd be better off with raw nuts and ground flaxseed than wasting your money on these cheap imitations.

--Worries about liver toxicity--A day doesn't go by that I don't have at least several questions about suffering toxic liver effects from niacin, vitamin D, statin drugs, etc. I have treated thousands of patients for heart disease in its various stages and forms and have used many different strategies. How many times have I seen serious liver toxicity? A handful of times and usually from either mis-use of the agent or drug, or in a person with several other coexisting diseases. (Other serious health conditions, like kidney failure, raise the toxicity of drugs and supplements.) Liver toxicity in the vast majority of otherwise healthy people is close to being a non-concern.

Readers of The Heart Scan Blog and of the Track Your Plaque website know that I celebrate expansion of knowledge and information access to the public. However, I am concerned that the flip side of this growing self-empowerment is expanding potential for mistakes. It reminds me of an attorney friend, who, when diagnosed with prostate cancer, explored all manner of alternative treatments, from laetrile to heavy metal chelation to high-dose lycopene tablets. At the initial stage of diagnosis, his cancer was readily treatable. He now has widely metastatic cancer.

Maintain an open mind, but think before you commit to some crazed claim of cure, some "secret" to health, somebody's brazen but concealed attempt at steering profits in their direction.

With freedom comes responsibility. Otherwise, you might be looking for love . . .oops, I mean health . . . in all the wrong places.

Track Your Plaque APB

9. February 2008 William Davis (7)

I'm posting this intriguing comment from the Track Your Plaque Member Forum because I would like to speak to the Member who posted it.

The Member said:

I tested at 965 last year, and while I have followed the TYP diet and nutraceutical recommendations, I was totally unprepared for my first repeat scan (at the same lab/machine) on January 29, 2008. My result was 4.0, and at first I assumed the rating scale had been changed.

I then noted that 3 of the big four arteries received scores of 0, which means the same in any scale, and that four nodules had disappeared from the scan field.

Wow!!

If this is true, it would represent the biggest success in the Track Your Plaque program--ever! It would be an incredible story to tell, to convince the public and medical community that it is indeed possible, and a cause for popping a bottle of champagne! It would also represent what I would regard as essentially a cure for coronary atherosclerosis, a virtual elimination.

While we have plenty of success in stopping the progression or reducing heart scan scores, we do not have 100% success. I wish we did. The Track Your Plaque program is, to some degree, a work in progress. We learn from experiences, continually adjust to obtain the results we desire. Even as it stands today, the Track Your Plaque program is superior to any program of heart disease prevention known--by a long stretch. But it's not infallible, it's not foolproof.

That's all the more reason I would like to communicate with the Track Your Plaque Member who posted this comment. I would also like permission to view the heart scans themselves. (I can't obtain them nor view them without the individual's permission.) While we often have difficulty judging reversal just by looking at heart scans, presumed reversal to this profound degree should be obvious, even to the naked eye.

I would like to know--in detail--precisely what steps were taken and whether there was anything unique about this person's medical history or in the program they followed. This is all in an effort to learn and help others do the same.

If you are the Member who posted this comment, I would like to hear more. Please post your further thoughts on the Track Your Plaque Member Forum, or privately through our Contact page . Or e-mail us at contact@cureality.com.

Vitamin D toxicity

6. February 2008 William Davis (26)

It is the craziest thing.

The notion of vitamin D being easily and readily toxic has grabbed hold of many people, including my colleagues who were taught that vitamin D was toxic in medical school based on the skimpiest (and often misinterpreted) observations in a handful of unusual cases.

In my practice and in the Track Your Plaque program, we routinely use doses of 2000-10,000 units per day, occasionally more. We are guided by blood levels of 25(OH) vitamin D3. I have personally never witnessed vitamin D toxicity.

Here's an interesting graph from Dr. Reinhold Vieth. Those of you familiar with the vitamin D argument know that Dr. Vieth is among the few genuine gurus in the vitamin D world.

From Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842-856. (Full text is available without charge.)

In the graph, the X's represent toxicity; circles fall within the non-toxic range. (Toxicity is generally defined as a level sufficient to raise blood calcium levels, "hypercalcemia.") Note that the 25(OH) vitamin D3 levels are given in nmol/L; to convert to ng/ml units that are customary in the U.S., divide the nmol/L value by a factor of 2.5.

You will notice that toxicity is virtually unheard of until the dose exceeds 10,000 units per day. Beyond 10,000 units per day, the curve heads upward sharply and toxicity does become a possibility, though not an absolute (since there are circles above 10,000 units).

You may also notice that the curve is relatively flat from vitamin D doses between 200 units and 10,000 units (log scale on x axis; arithmetic scale on y), the range of most common doses for vitamin D supplementation.

Another perspective on vitamin D blood levels is to examine the blood levels of people who are young and obtain plentiful sun exposure. Lifeguards, for instance, have blood levels of 84 ng/ml (210 nmol/L) without ill-effect. (Sun exposure cannot generate vitamin D toxicity, because of a feedback safety mechanism in skin.) While this may not represent an ideal level since they represent an extreme, it does provide reassurance that such levels are non-toxic. I also point out these levels occur in the youthful since most people lose 75% or more of vitamin D activating capacity in the skin by their 70s. Most of us over 40 are kidding ourselves if we think that a suntan provides sufficient vitamin D.

Keep in mind that it is not necessarily the dose of vitamin D that is toxic, but the blood level it generates. I take 10,000 units of vitamin D as a gelcap per day to maintain my blood level between 50-60 ng/ml (125-150 nmol/L). This strategy helps me keep my HDL in the 70-80 mg/dl range, my blood sugar around 90 mg/dl, my blood pressure <120/80, and I no longer experience colds nor winter "blues."

Copyright 2008 William Davis, MD

Turning plaque into profit

3. February 2008 William Davis (7)

For reasons unknown to me, I received a solicitation to invest in a company called Prescient Medical, with a slogan that caught my eye:

Detect and treat heart attacks before they occur.

The glossy brochure details their technology development strategy:

Predict(TM) Optical Catheter System--A catheter introduced into the coronary artery during a catheterization procedure to determine whether a specific plaque or vessel area is "vulnerable," i.e., prone to rupture in future.

Protect(TM) Luminal Shield--A stent-like metal device deployed into the coronary artery at the region of vulnerable plaque to prevent future plaque rupture.

The company anticipates FDA approval for their systems by 2009 and sales to begin by 2010. They predict sales of $7 billion.

Let's stop and think about this for a moment. It seems to me that, rather than pursuing the market of another stent for a "severe blockage," this company is going after the untapped procedural market of vulnerable plaque. In other words, their technology (an optical sensor technology that emits and analyzes light wavelengths to map specific plaque characteristics) identifies plaque that may rupture in months or years, followed by implantation of stent(s) that presumably prevent plaque rupture.

Thus, conceivably, many 20%, 30%, 40% etc. "blockages", atherosclerotic plaques that do not block flow and thereby pose no need for a conventional stent, will end up with this new type of stent. One patient could therefore receive multiple "Luminal Shields" in a single procedure.

When would these devices be employed? One pathway I could conceive of that my colleagues will be sure to exploit is 1) identify plaque by CT angiography, then 2) bring patient to the catheterization laboratory and perform this procedure for whatever hot, vulnerable plaques are identified. In other words, symptoms are no longer necessary. Reduced blood flow is no longer necessary. An abnormal stress test is no longer necessary. All that is required is that you have plaque. If the plaque is then determined to be vulnerable, then it is stented.

What bothers me about all this is the emerging effort to exploit this untapped market--a big one--of early heart disease as identified by coronary atherosclerotic plaque. As heart scans have demonstrated, there is an enormous amount of hidden heart disease in this world. This company has discovered a way to turn plaque into a profit opportunity, much as the statin drug industry found a way to "turn cholesterol into money."

The conventional stent market has plateaued and now has been, to some degree, battered by the drug-coated stent argument. Prescient has found a new and significant market for procedures and stents.

Is this really necessary? Why does plaque have to become a procedural disease? Doesn't it make more sense that, if vulnerable plaque is identified, that clinical trials are then designed to develop treatment strategies that modify vulnerable characteristics? Shockingly, this has not been done to any significant extent. Instead, the easiest path to a profit opportunity is to implant a "Luminal Shield."

You and I are able to inactivate, disempower, and essentially shut down plaque, while others are working furiously to convert it into a procedural profit opportunity. I personally find this so distasteful that I would sooner endorse a high-dose statin strategy than this approach.

You can view a video of my colleague, Dr. Martin Leon, on the Prescient Medical website, (or click here to go directly to the video), talking about how this technology will "change the treatment paradigm of the interventionalist from reactive to proactive." Scary stuff. Dr. Leon has made millions of dollars (probably more like tens of millions of dollars) from his support of technology companies for the interventional coronary device market.

My hope is that word of the sorts of techniques we use in the Track Your Plaque program disseminate before this sort of luminal coating idiocy gets off the ground.

(In actuality, a different version of this approach has been available for years using intravascular ultrasound (IVUS), another procedure that involves threading a catheter down each coronary artery during a catheterization procedure. IVUS can also cross-sectionally map a plaque's anatomy and identify "vulnerable" features, like a thin cap overlying a collection of semi-liquid fat ("lipid pool"). There has been some discussion of using this approach to identify vulnerable plaque followed by stent implantation, but it has never gotten off the ground and has certainly not found validation in any clinical study. By the way, any stent prevents plaque rupture, since by their very nature, the plaque contents are compressed, modified, and excluded to the exterior of the stent. Plaque rupture within a stent is very rare in its few millimeters of length. It may therefore not require some new technology to prevent plaque rupture.)

Statin mono-failure

1. February 2008 William Davis (6)

Evan's first heart scan score in November, 2006 yielded a high score for a 56-year old male: 542.

So he put up little fuss when his doctor prescribed simvastatin at a high dose.

Evan's LDL cholesterol before simvastatin: 158 mg/dl

Evan's LDL cholesterol on simvastatin: 72 mg/dl.

By conventional standards, Evan has had an excellent response. The rest of his lipid (cholesterol) panel was unrevealing: HDL 62 mg/dl, triglycerides 78 mg/dl. Evan doesn't smoke, has a normal blood pressure, and he is not diabetic. That should do it, right?

So his doctor thought. So Evan asked if another heart scan was in order. In December, 2007, after one year of simvastatin, his second heart scan score: 705--a 30% increase over one year.

Recall that, with no effort at prevention whatsoever, the natural progression of heart scan scores is a 30% per year increase. Did simvastatin do nothing?

This is quite typical of people who do nothing more than take a statin drug. While some people do slow plaque growth (we say "decelerate") modestly on a statin drug, Evan's experience is not unusual: plaque continues to grow despite high-dose statin drug and an apparently favorable cholesterol panel.

In fact, I can count the number of people who reduced their heart scan scores taking a statin drug alone on one finger.

Statins do not represent a cure for heart disease. They cannot be used as sole therapy to reduce risk for heart attack. In fact, given sufficient time, the majority of people who do nothing more than follow this standard line of treatment (along with the equally lame low-fat diet, etc.) will have done nothing more than postpone their heart attack. Elimination of risk? Nope.

This is among the reasons we developed the Track Your Plaque approach. While not foolproof, I know of no better approach to seize control over plaque growth.

Additional conversations on clinical studies which, as with Evan's experience, demonstrated how statin drugs fail to slow plaque growth can be found in previous Heart Scan Blog posts:

Don't be satisfied with "deceleration"

Study review: Yet another Lipitor study

Copyright 2008 William Davis, MD

Triglyceride traps

31. January 2008 William Davis (17)

Triglycerides are a potent trigger for coronary plaque growth.

Triglycerides in and of themselves probably do not cause plaque growth. Instead, triglycerides contribute to the formation of abnormal lipoproteins in the blood that, in turn, trigger coronary plaque, like VLDL, intermediate-density lipoprotein (IDL), and small LDL. Excess triglycerides also modify HDL structure and cause you to lose HDL in the urine.

I see plenty of people who begin with triglycerides of 200 mg/dl, 300, 700, even over 1000 mg/dl. It doesn't take long before you learn what works, what doesn't to reduce triglycerides. This is especially true in the Track Your Plaque approach, in which our target for triglycerides is 60 mg/dl or less.

Here's a list of things to consider if you are trying to gain control of your triglycerides:

--Fish oil--A mainstay of treatment. The omega-3 fatty acids from fish oil are the number one most potent treatment for high triglycerides.

--Reduction of high-glycemic index foods--Most notably wheat. Everybody knows that we shouldn't eat Snickers bars or bags of licorice. But many people eat plenty of wheat-containing breads, pastas, pretzels, crackers, breakfast cereals, etc., all in the name of increasing whole grains and fiber. In reality, they are causing triglycerides to skyrocket, dropping HDL, forming small LDL, increaaing blood sugar and blood pressure, and increasing obesity.

--Eliminating fructose and high-fructose corn syrup--This ubiquitous sweetener is now consumed in enormous quantities by the average American, nearly 80 lbs per year per person. You'll find it in soft drinks, ketchup, beer, breads, breakfast cereals, and many other processed foods. You'll find none in green peppers, cucumbers, and raw nuts. Fructose causes large rises in triglycerides, as well as diabetic patterns. Don't let "fat-free" claims fool you. Take a look at the ingredients in Kraft Fat-Free Caesar Italian salad dressing, for instance:

Kraft Fat-Free Caesar Italian

Ingredients:
Water, Vinegar, High Fructose Corn Syrup, Corn Syrup, Salt, Parmesan Cheese, Part-Skim Milk, Cheese Culture, Salt, Enzymes, Contains less than 2% of Garlic, Whey, Onion Juice, Autolyzed Yeast Extract, Phosphoric Acid, Worcestershire Sauce, Vinegar, Molasses, Corn Syrup, Water, Salt, Caramel Color, Dried Garlic, Sugar ,Spices, Tamarind, Natural Flavors, Hydrolyzed Soy Protein, Xanthan Gum, Potassium Sorbate and Calcium Disodium EDTA as Preservatives, Dried Garlic, Buttermilk, Spice, Dried Parsley, Caramel Color, Sodium Phosphate, Oleoresin Paprika.

--Alcohol--While a couple of drinks a day raises HDL, exerts anti-inflammatory effects, and reduces blood pressure, more than this begins to raise triglycerides. Although I've come across no formal studies on this question, my gut sense is that beer, in particular, raises triglycerides more than wine or other alcoholic beverages. Could it be the wheat source of beer? Or its high-fructose corn syrup? I don't know, but beer is the least desirable form of alcohol of the choices we have.

Following these simple steps, it is unusual in my experience that you cannot achieve a triglyceride level <60 mg/dl. Rarely do we need to add fibrate drugs or other prescription agents to reduce triglycerides.

Copyright 2008 William Davis, MD

High-dose fish oil for Lp(a)

30. January 2008 William Davis (16)

Lipoprotein(a), or Lp(a), is a problem area in coronary plaque reversal.

While our current Track Your Plaque record holder for largest percentage reduction in heart scan score has Lp(a), it remains among the more troublesome lipoprotein patterns.

One unique treatment for Lp(a) is high-dose omega-3 fatty acids from fish oil. While the data are relatively meager, there is one solid study from Lp(a) expert, Dr. Santica Marcovina of the University of Washington, called "The Lugalawa Study."

In this unique set of observations, 1300 members of a Bantu tribe living in Tanzania were studied. What made this population unusual is the fact that two groups of Bantus lived under different circumstances. One group lived on Nyasa Lake (3rd largest lake in Africa and reputed to have the greatest number of species of fish of any lake in the world) and ate large quantities of freshwater fish providing up to 500 mg of omega-3s, EPA and DHA, per day. Another Bantu group lived away from the lake as farmers, eating a pure vegetarian diet without fish.

Nyasa Lake

This situation among genetically similar stock provided a unique learning opportunity, a chance to assess whether different diets influenced Lp(a) levels.

The results: The fish-eating Bantus had an average Lp(a) level of 14.0 mg/dl. The farming, non-fish eating Bantus had an average Lp(a) of 27.0--a 48% difference. Curiously, a comparison of the apo(a) component of Lp(a) between the groups also showed that the fisherman expressed fewer dangerous small apo(a) forms, despite equal potential to express both.

The Lugalawa Study opens the question of whether similar results can be obtained not by moving to Tanzania and fishing Nyasa Lake, but by mimicking their experience by supplementing high doses of omega-3 fatty acids.

It's an intriguing question. In the Track Your Plaque program, we have no specific experience with this strategy, but it is certainly worth exploring further.

Watch for two upcoming Special Reports on the Track Your Plaque website in which we will be detailing 1)unique strategies for Lp(a) reduction, and 2) the usefulness of high-dose fish oil for coronary plaque reversal.

Interesting enough for a Virtual Clinical Trial?

Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

The many faces of LDL

29. January 2008 William Davis (0)

Pam has an LDL cholesterol of 144 mg/dl.

To most people, this means that she has a mildly elevated LDL value. Many people would respond by cutting the saturated fat in their diet. Most physicians would concur and talk about prescribing a statin drug.

Let me tell you what an LDL cholesterol of 144 mg/dl means to me:

1) It could mean an LDL of all large particles (which is good) or an LDL of all small particles (which is very bad). Or, perhaps it's some combination of big and small. I can't tell which just by knowing that LDL is 144.

Small LDL responds to a diet reduced in processed carbohydrates and wheat flour; large LDL does not. Small LDL responds in an exagerrated way to niacin; large LDL does not. It makes a difference.

2) It could mean that, hidden within LDL, is lipoprotein(a), or Lp(a). Recall that Lp(a) is a high-risk genetic pattern that can provide the false appearance of high LDL cholesterol. If Pam were prescribed a statin drug, it would have little effect and little benefit. (See Red flags for Lipoprotein(a).)

Knowing that Pam has Lp(a) can point us in an entirely different direction than just LDL cholesterol. It might mean high-dose fish oil, a more serious approach to niacin, hormonal treatments like DHEA or testosterone. It might mean more attention to warning your children about the possibility that they, too, might share this genetic trait.

3) It could mean both small LDL and Lp(a) are present simultaneously, an especially dangerous combined pattern that is among the highest risks for heart disease known.

4) Because Pam's LDL of 144 mg/dl was not measured, but calculated, it means that it is subject to tremendous inaccuracy.

In my office, calculated LDL cholesterols can be inaccurate by 50 or 100 mg/dl--commonly. So Pam's LDL of 144 mg/dl could really be 70 mg/dl, or it could be 244 mg/dl. Once again, it's a big difference.

Just like The Three Faces of Eve, the 1957 film in which Joanne Woodward played the three wildly different sides of Eve's personality--the daytime Eve White, the fun-loving and daring Eve Black, and Jane--so can LDL assume several different faces, all with different personalities, different implications.

Accepting LDL cholesterol as LDL cholesterol is a fool's game. It is only a starting point, nothing more. Accepting a statin drug based on LDL is, likewise, a trap fraught with uncertainty, the potential for limited or ineffective results, the price being your heart and health.

Condition Afflicts Millions: Do you have “YBS”?

We Need More.....Kettlebell

Thyroid and the gut: Hidden health partners

Omega-3 fatty acids likely NOT associated with prostate cancer

Are statins and omega-3s incompatible?

DHA: the crucial omega-3

Krill oil: Do the math

What tests are MORE important than cholesterol?

Cranberry Sauce

Apple Cranberry Crumble

CRP and Jupiter