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

High blood pressure vanquished

19. January 2011 William Davis (28)

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado

Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

16. January 2011 William Davis (25)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

15. January 2011 William Davis (13)

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl

I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

14. January 2011 William Davis (35)

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.

1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.

Restaurant eating: A fructose landmine

13. January 2011 William Davis (25)

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

12. January 2011 William Davis (15)

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

11. January 2011 William Davis (14)

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

10. January 2011 William Davis (29)

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

9. January 2011 William Davis (26)

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

6. January 2011 William Davis (0)

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.