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.

All posts by william-davis

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,

Kitchen sink approach for Lp(a)

29. August 2008 William Davis (12)

Lipoprotein(a), Lp(a), can be a tough nut to crack.

Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern.

I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people.

Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others.

Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a).

Even with this multi-agent approach, not everybody gains control over Lp(a).

That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).

While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on.

Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency.

There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years.

Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.

Making Dr. Friedewald an honest man

28. August 2008 William Davis (3)

Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L.

Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)

In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day.

By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.

So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc.

Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction.

Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number.

It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.

The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug.

As I've warned many times before: Beware the Friedewald calculated LDL.

Some basic vitamin D issues

24. August 2008 William Davis (7)

The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health.

Anne said:

I think it is important to stress that vitamin D supplementation needs to be continued long term.

I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times.

Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking?

If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life.

Twinb asked:

How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?

We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level.

Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level.

Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests?

Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute.

Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)

Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.

“How much vitamin D should I take?”

22. August 2008 William Davis (17)

It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong.

The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”

Utter nonsense.

The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach.

Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child.

It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors.

It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place.

As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized.

Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t.

Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.)

With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody.

Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved.

Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined.

But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)

Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized.

There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level.

Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period.

Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it.

I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor.

If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.)

So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)

You probably don't take enough fish oil

20. August 2008 William Davis (17)

The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:

Zero--I don't take any
17 (7%) of respondents

Less than 1000 mg per day
24 (10%) of respondents

1000-2000 mg per day
91 (38%) of respondents

2000-3000 mg per day
44 (18%) of respondents

3000-4000 mg per day
40 (16%) of respondents

More than 4000 mg per day
20 (8%) of respondents

Based on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more.

Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans.

But what dose is sufficient? What dose is ideal?

Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.)

If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary.

But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque?

This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:

--The Inuits (aka Eskimos) of Greenland and northern Canada
--The Japanese
--The Bantus of Tanzania who live along Nyasa Lake

All three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)).

The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids.

I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change.

We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change.

As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.

Vitamin D and HDL

19. August 2008 William Davis (23)

Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies

At first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduce
processed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL.

Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke.

Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so.

Add niacin, HDL increases another 5-10 mg/dl.

Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great.

Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl.

The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl.

Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude.

Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation.

Why? How?

That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.

An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years?

Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)