1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.
2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.
He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association's advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.
In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:
--Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.) --Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.) --Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)
Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?
I fear we don't have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.
Of the two omega-3 fatty acids that are best explored, EPA and DHA, it is likely DHA that exerts the most blood pressure- and heart rate-reducing effects. Here are the data of Mori et al in which 4000 mg of olive oil, purified EPA only, or purified DHA only were administered over 6 weeks:
In this group of 56 overweight men with normal starting blood pressures, only DHA reduced systolic BP by 5.8 mmHg, diastolic by 3.3 mmHg.
While each omega-3 fatty acid has important effects, it may be DHA that has an outsized benefit. So how can you get more DHA? Well, this observation from Schuchardt et al is important:
DHA in the triglyceride and phospholipid forms are 3-fold better absorbed, as compared to the ethyl ester form (compared by area-under-the-curve). In other words, fish oil that has been reconstituted to the naturally-occurring triglyceride form (i.e., the form found in fresh fish) provides 3-fold greater blood levels of DHA than the more common ethyl ester form found in most capsules. (The phospholipid form of DHA found in krill is also well-absorbed, but occurs in such small quantities that it is not a practical means of obtaining omega-3 fatty acids, putting aside the astaxanthin issue.)
So if the superior health effects of DHA are desired in a form that is absorbed, the ideal way to do this is either to eat fish or to supplement fish oil in the triglyceride, not ethyl ester, form. The most common and popular forms of fish oil sold are ethyl esters, including Sam's Club Triple-Strength, Costco, Nature Made, Nature's Bounty, as well as prescription Lovaza. (That's right: prescription fish oil, from this and several other perspectives, is an inferior product.)
What sources of triglyceride fish oil with greater DHA content/absorption are available to us? My favorites are, in this order:
Ascenta NutraSea CEO and founder, Marc St. Onge, is a friend. Having visited his production facility in Nova Scotia, I was impressed with the meticulous methods of preparation. At every step of the way, every effort was made to limit any potential oxidation, including packaging in a vacuum environment. The Ascenta line of triglyceride fish oils are also richer in DHA content. Their NutraSea High DHA liquid, for instance, contains 500 mg EPA and 1000 mg DHA per teaspoon, a 1:2 EPA:DHA ratio, rather than the more typical 3:2 EPA:DHA ratio of ethyl ester forms.
Pharmax (now Seroyal) also has a fine product with a 1.4:1 EPA:DHA ratio.
Nordic Naturals has a fine liquid triglyceride product, though it is 2:1 EPA:DHA.
The manufacturers of krill oil claim that the phospholipid form of omega-3 fatty acids, EPA and DHA, enhance their absorption. There are indeed some data to that effect:
Here are some representative krill oil preparations available on the market:
MegaRed Krill Oil: EPA 50 mg DHA 24 mg Total omega-3s (EPA + DHA + other forms) 90 mg Price: $28.99 for 60 softgels
Source Naturals (a fine company otherwise, by the way):
EPA 150 mg DHA 90 mg Total omega-3 fatty acids 300 mg Price: $24.99 for 60 softgels
Alright, let's do some simple math:
Average volume of blood in the human body (all components): 5000 cc Percentage of red blood cells (RBCs) by volume: 45% Total volume RBCs: 2250 cc Percentage of total volume RBCs occupied by fatty acids:
In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.
So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.
But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:
--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.
Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.
--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.
--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.
HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.
--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.
Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).
--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.
Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.
All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.
Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque! Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.
There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.
1 cup water 12 ounces fresh whole cranberries Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía) 1 tablespoon orange zest + juice of half an orange ½ cup chopped walnuts 1 teaspoon ground cinnamon ½ teaspoon ground nutmeg ¼ teaspoon ground cloves
In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.
Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.
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.
