Biscuits and Gravy



Biscuits and gravy: the ultimate comfort food . . . one you thought you’d never have again!

The familiar dish of breakfast and holiday meals is recreated here with a delicious gravy that you can pour over piping hot biscuits. Because it contains no wheat or other unhealthy thickeners like cornstarch made with “junk” carbohydrates, there should be no blood sugar or insulin problems with this dish, nor joint pain, edema, acid reflux, mind “fog,” or dandruff—life is good without wheat!

While the gravy is also dairy-free for those with dairy intolerances, the biscuits are not, as there are cheese and butter in the biscuits, both of which are optional, e.g., leave out the cheese and replace butter with coconut or other oil.

Makes 10 biscuits

Gravy:
2 tablespoons extra-virgin olive oil
1 pound loose sausage meat
2½ cups beef broth
¼ cup coconut flour
½ cup coconut milk (canned variety)
1 tablespoon onion powder
1 teaspoon garlic powder
½ teaspoon sea salt
Dash ground black pepper

Biscuits:
1 cup shredded cheddar (or other) cheese
2 cups almond meal/flour
¼ cup coconut flour
¾ teaspoon baking soda
½ teaspoon sea salt
2 large eggs
4 ounces butter, melted (or other oil, e.g., extra-light olive, coconut, walnut)

To make gravy:
In large skillet, heat oil over medium heat. Sauté sausage, breaking up as it browns. Cook until thoroughly cooked and no longer pink.

Turn heat up to medium to high and pour in beef broth. Heat just short of boiling, then turn down to low heat. Stir in coconut flour, little by little, over 3-5 minutes; stop adding when gravy obtains desired thickness. Pour in coconut milk and stir in well. Add onion powder, garlic powder, salt, and pepper and simmer over low heat for 5 minutes. Add additional salt and pepper to taste. Remove from heat and set aside.

To make biscuits:
Preheat oven to 325° F.

In food chopper or processor, pulse shredded cheese to finer, granular consistency.

Pour cheese into large bowl, then add almond meal, coconut flour, baking soda, and salt and mix thoroughly. Add the eggs and butter or oil and mix thoroughly to yield thick dough.

Spoon out dough into 10 or so ¾-inch thick mounds onto a parchment paper-lined baking pan. Bake for 20 minutes or until lightly browned and toothpick withdraws dry.

Ladle gravy onto biscuits just before serving.

The Perfect Carnivore

People who carry the gene for lipoprotein(a), Lp(a), tend to be:

--Intelligent--The bell curve of IQ is shifted rightward by a substantial margin.
--Athletic--With unusual capacity for long-endurance effort, thus the many marathoners, triathletes, and long-distance bikers with Lp(a).
--Tolerant to dehydration
--Tolerant to starvation
--Resistant to tropical infections

In other words, people with Lp(a) have an evolutionary survival advantage. More than other people, they make clever, capable hunters who can run for hours to chase down prey, not requiring food or water, and less likely to succumb to the infections of the wild. In a primitive setting, people with Lp(a) are survivors. Evolution has likely served to select Lp(a) people for their superior survival characteristics.

But wait a minute: Isn't Lp(a) a risk for heart attack and stroke? Don't we call Lp(a) "the most aggressive known cause for heart disease and stroke that nobody gives a damn about"?

Yes. So what allows this evolutionary advantage for survival to become a survival disadvantage?

Carbohydrates, especially those from grains and sugars. Let me explain.

More so than other people, Lp(a) people express the small LDL pattern readily when they consume carbohydrates such as those from "healthy whole grains." Recall that the gene for Lp(a) is really the gene for apoprotein(a), the protein that, once produced by the liver and released into the bloodstream, binds to an available LDL particle to create the combination Lp(a) molecule. If the LDL particle component of Lp(a) is small, it confers greater atherogenicity (greater plaque-causing potential). Thus, carbohydrate consumption makes Lp(a) a more aggressive cause for atherosclerotic plaque. The situation can be made worse by exposure to vegetable oils, such as those from sunflower or corn, which increases production of apo(a).

Also, more than other people, Lp(a) people tend to show diabetic tendencies with consumption of carbohydrates. Eat "healthy whole grains," for instance, or if a marathoner carb-loads, he/she will show diabetic-range blood sugars. I have seen long-distance runners or triathletes, for instance, have a 6 ounce container of sugary yogurt and have blood sugars of 200 mg/dl or higher. The extreme exercise provides no protection from the diabetic potential.

Because carbohydrates are so destructive to the Lp(a) type, it means that people with this pattern do best by 1) absolutely minimizing exposure to carbohydrates and vegetable oils, ideally grain-free and sugar-free, and 2) rely on a diet rich in fats and proteins.

The perfect diet for the Lp(a) type? It would be a diet of feasting on the spoils of the hunt, devouring the wild boar captured and slaughtered and eating the snout, hindquarters, spleen, kidneys, heart, and bone marrow, then eating mushrooms, leaves, nuts, coconut, berries, small rodents, reptiles, fish, birds, and insects when the hunt is unproductive.

Capable hunter, survivor, consumer of muscle and organ meats: I call people with Lp(a) "The Perfect Carnivores."

Track Your Plaque in the news

The NPR Health Blog contacted me, as they were interested in learning more about health strategies and tools that are being used by individuals without their doctors. The Track Your Plaque website and program came up in their quest, as it is the only program available for self-empowerment in heart disease.

Several Track Your Plaque Members spoke up to add their insights. The full text of the article can be viewed here.

How's Your Cholesterol? The Crowd Wants To Know
Mainstream medicine isn't in favor of self-analysis, or seeking advice from non-professionals, of course. And anyone who does so is running a risk.

But there are folks who want to change the course of their heart health with a combination of professional and peer support. Some are bent on tackling the plaque that forms in arteries that can lead to heart disease. They gather online at Track Your Plaque, or "TYP" to the initiates.

"We test, test, test ... and basically experiment on ourselves and have through trial and error came up with the TYP program, which is tailored to the individual," Patrick Theut, a veteran of the site who tells Shots he has watched his plaque slow, stop and regress.

The site was created in 2004 by Bill Davis, a preventive cardiologist in Milwaukee, Wisc. Davis is also the author of Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health, which argues that wheat is addictive and bad for most people's health. Davis recommends eliminating wheat from the diet to most new members of Track Your Plaque.

"The heart is one of the hardest things to self-manage but when you let people take the reins of control, you get far better results and far fewer catastrophes like heart attacks," Davis tells Shots.

Doctors typically give patients diagnosed with heart disease two options: take cholesterol-lowering statin drugs, or make lifestyle changes, like diet. It's usually far easier for both parties — the doctor and the patient — to go with the drugs than manage the much more difficult lifestyle changes, Davis says.

"Doctors say take the Lipitor, cut the fat and call me if you have chest pain," he explains. "But that's an awful way to manage care."

TYP has members submit their scores from heart CT scans, cholesterol values, lipoproteins and other heart health factors to a panel of doctors, nutritionists and exercise specialists. Then they receive advice in the form of an individualized plaque-control program. But the online forum, where users share their results with other members and exchange tips, is where most of the TYP action happens.

The community currently has about 2,400 members who pay $39.95 for a quarterly membership, or $89.75 for a yearly membership. Davis says all proceeds go towards maintaining the website.

Ilaine Upton is a 60-year-old bankruptcy lawyer from Fairfax, Va., and a TYP member. At a friend's suggestion, Upton decided to get a heart CT scan in July. Her score was higher than it should have been (22 instead of 0), so she decided to get her blood lipids and cholesterol tested, too, and sent a sample off to MyMedLabs.com.

She learned that her LDL particle count was over 2,000 ("crazy high," she says), and she posted her results on TYP. Davis advised her that a low-carb diet would reduce it, so she decided to try it.

Since July, she says she has had "excellent results" with the program, and her LDL counts are coming down.

"It would be nice to have a [personal] physician involved in this, but [my insurer] Blue Cross won't pay if you are not symptomatic, and I am trying to prevent becoming symptomatic," says Upton. "I feel very empowered by this knowledge and the ability to take better control of my health by getting feedback on the decisions I make."

Pecan Streusel Coffee Cake


This is about as decadent as it gets around here!

Here’s a recreation of an old-fashioned coffee cake, a version with a delicious chewy-crunchy streusel topping.

I’ve specified xylitol as the sweetener in the topping, as it is the most compatible sweetener for the streusel “crumb” effect and browning.

Variations are easy. For example, for an apple pecan coffee cake, add a layer of finely-chopped or sliced apples to the cake batter and topping.

Additional potential carbohydrate exposure comes from the garbanzo bean flour and molasses. However, distributed into 10 slices, each slice provides 7.2 grams “net” carbs (total carbs minus fiber), a perfectly tolerable amount. Be careful not to exceed two slices!

Yield 10 slices

Cake:
2½ cups almond flour
½ cup garbanzo bean flour
1 tablespoon ground cinnamon
1 teaspoon baking soda
Sweetener equivalent to ¾ cup sugar
Dash sea salt

3 eggs separated
3/8 teaspoon cream of tartar
1 tablespoon vanilla extract
4 ounces butter, melted
Juice of ½ lemon

Topping:
½ cup almond flour
¼ cup pecans, finely chopped
1 tablespoon ground cinnamon
½ cup xylitol
1 tablespoon molasses
6 ounces butter, cut into ½-inch widths, at room temperature

Preheat oven to 325º F. Grease bread pan.

In bowl, combine almond flour, garbanzo flour, cinnamon, baking soda, sweetener, salt, and mix.

In small bowl, whip egg whites and cream of tartar until stiff peaks form. At low speed, blend in egg yolks, vanilla, melted butter, and lemon juice.

Pour liquid mixture into almond mixture and mix thoroughly. Pour into microwave-safe bread pan and microwave on high for 3 minutes. Remove and set aside.

To make topping, combine almond flour, pecans, cinnamon, xylitol, and molasses in small bowl and mix. Mix in butter

Spread topping on cake. Bake for 20 minutes or until toothpick withdraws dry.

Recipe: Peanut Butter and Jelly Macaroons



If you miss peanut butter and jelly sandwiches, you’re going to absolutely love these peanut butter and jelly macaroons!

Not everybody loves the taste or texture of coconut. This issue is solved by the first step: toasting shredded coconut, then reducing them down to a granular consistency. This yields a macaroon consistency without the dominant coconut taste, replaced instead with the flavors of PB & J.

I’ve specified liquid stevia as the sweetener, but this is easily replaced by your choice of sweetener. Note that, regardless of which sweetener used, they vary in sweetness from brand to brand and the quantity required to equal the ½ cup of sugar equivalent can vary. It always helps to taste your batter and adjust sweetness.

Also, I used Swerve in this recipe, the erythritol-inulin mix that enhances texture, but its use is optional.

As written, each macaroon contains just over 3 grams “net” carbohydrates (total carbs minus fiber), meaning you can have several before doing any damage!

Makes 24 macaroons

3 cups shredded unsweetened coconut
2 tablespoons vanilla extract
1 teaspoon almond extract
¼ cup coconut flour
¼ cup dried unsweetened cherries (or other unsweetened berries)
2 tablespoons coconut oil
¼ cup natural peanut butter, room temperature
2 egg whites
½ teaspoon liquid stevia or sweetener equivalent to ½ cup sugar
2 tablespoons Swerve


Preheat oven to 300° F.

In large bowl, combine coconut, vanilla and almond extracts, and mix.

Spread mixture on baking sheet and bake for 10 minutes, stirring occasionally, until very lightly browned. Be careful not to burn. Remove and cool. (Leave oven at 300° F.)

When cooled, using food chopper, food processor, or coffee grinder, pulse coconut mixture until coconut reduced to consistency of coffee grounds. Pour back into bowl. Stir in coconut flour.

Place cherries or other berries in food chopper, food processor, or coffee grinder and pulse until reduced to small granules or paste. Remove with spatula and add to coconut mixture. Set aside.

Place egg whites in bowl and whip until frothy and stiff peaks form.

In small microwave-safe bowl, combine coconut oil and peanut butter and microwave in 10-second increments until warm (not hot) liquid. Stir in egg whites, followed by stevia and Swerve, and blend thoroughly.

Dispense dough onto a parchment paper-lined baking sheet using a 1 ½-inch cookie scooper or spoons.

Bake for 15 minutes or until lightly browned.

I Wish I Had Lipoprotein(a)!

Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.


In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.

What WERE they thinking

When the Dietary Guidelines for Americans were drafted and the USDA and U.S. Department of Health and Human Services charged with disseminating this information to us . . .

When the American Heart Association created its Total Lifestyle Change (TLC) diet to reduce cardiovascular risk and reduce cholesterol . . .

When the American Diabetes Association developed its diet to help diabetics manage their blood sugars and prevent hypoglycemia . . .


How did conditions like Familial Hypertriglyceridemia fit into this scheme?

Green Tea Ginger Orange Bread

How about all the health benefits of green tea in wheat-free bread form, spiced up with the magical combined flavors of ginger and orange?

Frequent consumption of green tea accelerates loss of visceral (“wheat belly”) fat, increases HDL and reduces triglycerides, reduces blood pressure, and may provide cardiovascular benefits that go beyond these markers such as reduction of oxidative stress. In this Green Tea Ginger Orange Bread, we don’t just drink the tea—we eat it! This provides an even more powerful dose of the green tea catechins believed to be responsible for the health benefits of green tea.

You can grind your own green tea from dried bulk leaves or it can be purchased pre-ground. I’ve used sencha and matcha green tea varieties with good results. The Teavana tea store sells a Sencha preground green tea that works well. If starting with bulk tea leaves, pulse in your food chopper, food processor, or coffee grinder (cleaned thoroughly first!) to generate green tea powder. You will need only a bit, as a little goes a long way.

The entire loaf contains 26 grams “net” carbohydrates; if cut into 10 slices, each slice therefore yields 2.6 grams net carbs, a perfectly tolerable amount.


Bread:
1¼ cup almond meal/flour
½ cup coconut flour
2 tablespoons ground golden flaxseed
1 teaspoon baking powder
Sweetener equivalent to 1 cup sugar
1 tablespoon ground green tea
1½ teaspoons ground ginger
1½ teaspoons ground allspice
1½ ground cinnamon
2 large eggs, separated
¼ teaspoon cream of tartar
1 tablespoon vanilla extract
1 teaspoon almond extract
Grated zest from 1 orange + 2 tablespoons squeezed juice
1/2 cup coconut milk

Frosting:
4 ounces cream cheese, room temperature
1 teaspoon fresh lemon juice
Sweetener equivalent to 1 tablespoon sugar

Preheat oven to 350° F. Grease a 9” x 5” bread pan.

In large bowl, combine almond meal/flour, coconut flour, flaxseed, baking powder, sweetener, green tea, ginger, allspice, and cinnamon and mix.

In small bowl, whip egg whites and cream of tartar until stiff peaks form. At low mixer speed, blend in egg yolks, vanilla extract, almond extract, orange zest and juice, and coconut milk.

Pour egg mixture into almond meal/flour mixture and mix by hand thoroughly.

Pour dough into bread pan and place in oven. Bake for 40 minutes or until toothpick withdraws dry. Remove and cool.

For frosting, combine cream cheese, lemon juice, and sweetener and mix. When cooled, spread frosting over top of bread.

Chocolate Bomb Bars

These healthy bars will blast you with chocolate from several directions!

Look for cacao nibs in health food stores, Whole Foods Market, or at nuts.com. If unavailable, the bars are still delicious without them.



These bars contain around 4-5 grams "net" carbs per bar, well within the tolerance for most people.

Yields approximately 10 bars

1 cup ground almonds
2 tablespoons coconut flour
1 tablespoon unsweetened cocoa powder
1/2 cup cacao nibs
1/2 cup unsweetened shredded coconut
2 ounces 85-90% cocoa chocolate, finely chopped
3/4 cup raw pumpkin or sunflower seeds
Sweetener equivalent to 3/4 cup sugar
2 tablespoons almond butter
1/4 cup coconut milk
2 tablespoons coconut oil or cocoa butter (food grade)

Preheat oven to 200 degrees F. Lay sheet of parchment paper on large baking pan.

In large bowl, combine ground almonds, coconut flour, cocoa powder, cacao nibs, coconut, chocolate bits, pumpkin seeds, and sweetener (if dry) and mix.

In microwave-safe bowl or in small sauce pan, add almond butter, coconut milk, and coconut oil and sweetener (if liquid) and heat for 15 second increments in microwave until liquid, but not hot. If using stove, heat at low-heat enough to make liquid easily mixed, but not hot.

Pour liquid into dry almond mixture and mix together thoroughly. If too stiff, add water one tablespoon at at time until the consistency of thick dough.

Spoon out approximately 1 1/2-inch balls, shaping with the spoon and/or your hands into bar shapes.

Bake for 35 minutes. Remove and cool.

An iodine primer

What if your diet is perfect--no wheat, no junk carbohydrates like that from corn or sugars, you are physically active--yet you fail to lose weight? Or you hit a plateau after an initial loss?

First think iodine.

Iodine is an essential nutrient. It is no more optional than, say, celebrating your wedding anniversary or obtaining vitamin C. If you forget to do something nice for your wife on your wedding anniversary, I would fear for your life. If you develop open sores all over your body and your joints fall apart, you could undergo extensive plastic surgery reconstruction and joint replacement . . . or you could just treat the scurvy causing it from lack of vitamin C.

Likewise iodine: If you have an iodine deficiency, you experience lower thyroid hormone production, since T3 and T4 thyroid hormones require iodine (the "3" and "4" refer to the number of iodine atoms per thyroid hormone molecule). This leads to lower energy (since the thyroid controls metabolic rate), cold hands and feet (since the thyroid is thermoregulatory, i.e., temperature regulating), and failed weight loss. So iodine deficiency is one of the items on the list of issues to consider if you eliminate wheat with its appetite-stimulating opiate, gliadin, and high-glycemic carbohydrate, amylopectin A, and limit other carbohydrates, yet still fail to lose weight. A perfect diet will not fully overcome the metabolism-limiting effects of an underactive thyroid.

Given sufficient time, an enlarged thyroid gland, or goiter, develops, signaling longstanding iodine deficiency. (The treatment? Iodine, of course, not thyroid removal, as many endocrinologists advocate.) Your risk for heart attack, by the way, in the presence of a goiter is increased several-fold. Goiters are becoming increasingly common and I see several each week in my office.

Iodine is found in the ocean and thereby anything that comes from the ocean, such as seafood and seaweed. Iodine also leaches into the soil but only does so coastally. It means that crops and livestock grown along the coasts have some quantity of iodine. Humans hunting and foraging along the coast will be sufficient in iodine, while populations migrating inland will not.

It also means that foods grown inland do not have iodine. This odd distribution for us land dwelling primates means that goiters are exceptionally common unless iodine is supplemented. Up to 25% of the population can develop goiters without iodine supplementation, a larger percentage experiencing lesser degrees of iodine deficiency without goiter.

In 1924, the FDA became aware of the studies that linked goiters to lack of iodine, reversed with iodine supplementation. That's why they passed a regulation encouraging salt manufacturers to add iodine, thought to be an easy and effective means for an uneducated, rural populace to obtain this essential nutrient. Their message: "Use more iodized salt. Keep your family goiter free!" That was actually the slogan on the Morton's iodized salt label, too.

It worked. The rampant goiters of the first half of the 20th century disappeared. Iodized salt was declared an incredible public health success story. Use more salt, use more salt.

You know the rest. Overuse of salt led to other issues, such as hypertension in genetically susceptible people, water retention, and other conditions of sodium overexposure. The FDA then advises Americans to slash their intake of sodium and salt . . . but make no mention of iodine.

So what recurs? Iodine deficiency and goiters. Sure, you eat seafood once or twice per week, maybe even have the nori (sheet seaweed) on your sushi once in a while . . . but that won't do it for most. Maybe you even sneak some iodized salt into your diet, but occasional use is insufficient, especially since the canister of iodized salt only contains iodine for around 4 weeks, given iodine's volatile nature. (Iodized salt did work when everybody in the house salted their food liberally and Mom had to buy a new canister every few weeks.)

Iodine deficiency is common and increasing in prevalence, given the widespread avoidance of iodized salt. So what happens when you become iodine deficient? Here's a partial list:

--Weight loss is stalled or you gain weight despite your efforts.
--Heart disease risk is escalated
--Total and LDL cholesterol and triglyceride values increase
--Risk of fibrocystic breast disease and possibly breast cancer increase (breast tissue concentrates iodine)
--Gingivitis and poor oral health increase (salivary glands concentrate iodine)

(Naturopathic doctor Lyn Patrick, ND, has written a very nice summary available here.)

So how do you ensure that you obtain sufficient iodine every day? You could, of course, eat something from the ocean every day, such as coastal populations such as the Japanese do. Or you could take an inexpensive iodine supplement. You can get iodine in a multivitamin, multimineral, or iodine drops, tablets, or capsules.

What is the dose? Here's where we get very iffy. We know that the Recommended Daily Allowance (RDA), the intake to not have a goiter, is 150 mcg per day for adults (220 mcg for pregnant females, 290 mcg for lactating females). Most supplements therefore contain this quantity.

But what if our question is what is the quantity of iodine required for ideal thyroid function and overall health? Ah, that's where the data are sketchy. We know, for instance, that the Japanese obtain somewhere between 3,500 and 13,000 mcg per day (varying widely due to different habits and locations). Are they healthier than us? Yes, quite a bit healthier, though there may be other effects to account for this, such as a culture of less sweet foods and more salty, less wheat consumption, etc. There are advocates in the U.S., such as Dr. David Brownstein in Michigan, who argues that some people benefit by taking doses in the 30,000 to 50,000 mcg per day range (monitored with urinary iodine levels).

As is often the case with nutrients, we lack data to help us decide where the truly ideal level of intake lies. So I have been using and advocating intakes of 500 to 1000 mcg per day from iodine capsules, tablets, or drops. A very easy way to get this dose of iodine is in the form of kelp tablets, i.e., dried seaweed, essentially mimicking the natural means of intake that also provides iodine in all its varied forms (iodide, sodium iodate, potassium iodide, potassium iodate, iodinated proteins, etc.) This has worked out well with no ill effects.

The only concern with iodine is in people with Hashimoto's thyroiditis or (rarely) an overactive thyroid nodule. Anyone with these conditions should only undertake iodine replacement carefully and under supervision (monitoring thyroid hormone levels).

Iodine is inexpensive, safe, and essential to health and weight management. If it were a drug, it would enjoy repeated expensive marketing and a price tag around $150 per month. But it is an essential nutrient that enjoys none of the attention-getting advantages of drugs, and therefore is unlikely to be mentioned by your doctor, yet carries great advantage for helping to maintain overall health.

Green coffee bean extract in AGF Factor I

Track Your Plaque's new and proprietary formulation, AGF Factor I, is designed to to support a program to achieve low levels of endogenous glycation.

Endogenous glycation, discussed at length in a recent Track Your Plaque Special Report, makes LDL particles (especially small LDL particles) more prone to oxidation and thereby more atherogenic, i.e., more likely to contribute to atherosclerotic plaque. Endogenous glycation also exerts unhealthy effects on long-lived proteins in the body, such as the proteins in the lenses of your eyes (cataracts), the lining of arteries (hypertension), and the cartilage cells of joints (brittle cartilage and arthritis).

Endogenous glycation is reduced by slashing carbohydrates in the diet, especially the most offensive carbohydrates of all, the amylopectin A of wheat, sucrose, high-fructose corn syrup and other fructose sources. Endogenous glycation can also be blocked by using blockers of the glycation reaction, such as benfotiamine (lipid-soluble thiamine), pyridoxal-5'-phosphate (a form of vitamin B6 with greater glycation blocking effect), and chlorogenic acid from green coffee beans, all components of AGF Factor I, which also contains Portulaca oleracea (Portusana), or purslane, for reduction of glucose.

Green coffee bean extract, and thereby chlorogenic acid, is receiving increased attention, most recently due to a study demonstrating substantial weight loss with 750-1050 mg green coffee bean extract, providing approximately 325-500 mg chlorogenic acid per day. Participants lost 15.4 pounds over 8 weeks at the higher dose (500 mg chlorogenic acid per day), while participants lost 8.8 pounds over 8 weeks at the lower dose (325 mg chlorogenic acid per day).

AGF Factor I was not formulated for weight loss but, taken twice or three times per day, does indeed mimic the dose of chlorogenic acid from green coffee bean extract used in the weight loss study. If you wish to take advantage of this application of chlorogenic acid/green coffee bean extract, while also maximizing protection from endogenous glycation, our AGF Factor I is one excellent choice to do so.

Lessons learned from the 2012 Low-carb Cruise

I just returned from Jimmy Moore's Low-carb Cruise, a 7-day excursion to Jamaica, Grand Cayman Island, and Cozumel aboard the Carnival Magic. During our 7 wonderful days, a number of authors and experts spoke, each offering their unique perspective on the low-carb world. The focus was the science, experience, and practical application of low-carbohydrate diets.

The event kicked off with a roast by Tom Naughton of Fat Head fame, who entertained with his insightful low-carb humor and predictions of my demise at the hands of Monsanto!

Among the most important lessons provided:

Dr. Andreas Eenfeldt of the Diet Doctor blog discussed how Sweden is leading the world as the nation with the most vigorous low-carbohydrate following, witnessing incredible weight loss and reversal of carbohydrate-related diseases way ahead of the U.S. experience. I spent several hours with Dr. Eenfeldt who, besides being an engaging speaker, is a new father and an all-around gentleman. At 6 ft, 7 inches, he also towered high above all of us.

Dr. Eric Westman of Duke University and author of The New Atkins for a New You, debunked low-carbohydrate myths, such as "low-carb diets are high-protein diets that make your kidneys explode."

Dr. John Briffa, creator of the popular blog, Dr. John Briffa: A Good Look at Good Health, and author of the wonderfully straightforward primer to low-carbohydrate eating, Escape the Diet Trap, stressed the importance of never allowing hunger to rule behavior. Dr. Briffa's serious writing tone conceals an incredible charm and wit that took me by surprise, having spent several thoroughly engaging hours over breakfast, lunch, and dinner with him over the week.

Fred Hahn, exercise expert, founder of Serious Strength and author of Slow Burn Fitness Revolution and Strong Kids, Healthy Kids, debunked a number of trendy exercise methods, boiling many of the purported benefits of exercise down to that of increased strength.

Dr. Chris Masterjohn of The Daily Lipid and supporter of the Weston A. Price Foundation program, provided a comprehensive overview of the data that fails to link saturated fat with heart disease. He also helped me understand the analytical techniques used in studies of advanced glycation end-products.

Denise Minger, brilliant young usurper of China Study dogma and blogger at Raw Foods SOS, proved an engaging speaker and a truly real person (since some critics of her analyses have actually questioned whether there was even such a person!). She also proved every bit as likable as she seems in her captivating blog discussions.

Dr. Jeff Volek, prolific researcher from University of Connecticut, author of over 200 studies validating low-carbohydrate diet effects, and author of the recently released book with Dr. Stephen Phinney, The Art and Science of Low Carbohydrate Living, debunked myths behind carbohydrate dependence and "loading" by athletes. He also talked about how assessing blood ketones may be the gold standard method to ensure low-grade ketosis on a long-term low-carb effort.

Over a bottle of wine, Jimmy Moore and I reminisced over how his modest start with no experience in blogging or media has now ballooned to an audience of over 100,000 readers/viewers.

All in all, Jimmy's Low-carb Cruise experience was worth every minute, with many wonderful lessons and memories!

Chili Sesame Crackers

Looking for something hot and crunchy?

These chili sesame crackers are perfect for dipping into hummus or salsa. As written, the recipe yields a moderately spicy cracker that you can modify readily by increasing or decreasing quantities of cayenne pepper and Tabasco sauce.

This recipe uses sesame seeds as the "flour." Either brown sesame seeds or the lighter version work, though the lighter seeds yield a slightly less bitter flavor with the spices.

For ease of baking, a shallow baking pan measuring 11 x 17 inches works best, as it allows the batter to fill the pan and spread to a cracker thickness. With a smaller pan, you may have to bake in two batches.

Makes approximately 30 chips

2 cups raw sesame seeds
1 cup shredded Parmesan cheese
2 tablespoons extra-virgin olive oil
1 tablespoon chili powder
½ teaspoon cayenne pepper
2 teaspoons onion powder
1 teaspoon garlic powder
1 teaspoon dry mustard
1 teaspoon sea salt
1 teaspoon Tabasco sauce
1¼ cups water

Preheat oven to 350º F.

In food chopper or food processor, grind 1¼ cups sesame seeds to fine meal. Remove and place in large bowl.

Place shredded Parmesan cheese in food chopper or food processor and pulse briefly until reduced to granular consistency. Add to sesame seed meal and mix. Stir in olive oil.

Add remaining (unground) sesame seeds, chili powder, cayenne pepper, onion and garlic powder, mustard, sea salt and mix thoroughly. Add Tabasco sauce and water and mix. Add additional water, if necessary, one tablespoon at a time, to obtain a consistency similar to pancake batter.

Pour mixture into baking pan and smooth to fill pan and obtain a thickness of a cracker. If too thick, remove some batter and re-smooth. Optionally, roll a clean cylindrical glass or bottle over top to smooth and yield a consistent thickness.

Bake for 30 minutes or until edges browned and center firm. If a dry, extra crunchy cracker is designed, bake an additional 10-15 minutes at 250 degrees F.

Remove and allow to cool. Cut with pizza cutter to desired size.

Opiate of the masses

Although it is a central premise of the whole Wheat Belly argument and the starting strategy in the New Track Your Plaque Diet, I fear that some people haven't fully gotten the message:

Modern wheat is an opiate.

And, of course, I don't mean that wheat is an opiate in the sense that you like it so much that you feel you are addicted. Wheat is truly addictive.

Wheat is addictive in the sense that it comes to dominate thoughts and behaviors. Wheat is addictive in the sense that, if you don't have any for several hours, you start to get nervous, foggy, tremulous, and start desperately seeking out another "hit" of crackers, bagels, or bread, even if it's the few stale 3-month old crackers at the bottom of the box. Wheat is addictive in the sense that there is a distinct withdrawal syndrome characterized by overwhelming fatigue, mental "fog," inability to exercise, even depression that lasts several days, occasionally several weeks. Wheat is addictive in the sense that the withdrawal process can be provoked by administering an opiate-blocking drug such as naloxone or naltrexone.

But the "high" of wheat is not like the high of heroine, morphine, or Oxycontin. This opiate, while it binds to the opiate receptors of the brain, doesn't make us high. It makes us hungry.

This is the effect exerted by gliadin, the protein in wheat that was inadvertently altered by geneticists in the 1970s during efforts to increase yield. Just a few shifts in amino acids and gliadin in modern high-yield, semi-dwarf wheat became a potent appetite stimulant.

Wheat stimulates appetite. Wheat stimulates calorie consumption: 440 more calories per day, 365 days per year, for every man, woman, and child. (440 calories per person per day is the average.) We experience this, sense the weight gain that is coming and we push our plate away, settle for smaller portions, increase exercise more and more . . . yet continue to gain, and gain, and gain. Ask your friends and neighbors who try to include more "healthy whole grains" in their diet. They exercise, eat a "well-balanced diet" . . . yet gained 10, 20, 30, 70 pounds over the past several years. Accuse your friends of drinking too much Coca Cola by the liter bottle, or being gluttonous at the all-you-can-eat buffet and you will likely receive a black eye. Many of these people are actually trying quite hard to control impulse, appetite, portion control, and weight, but are losing the battle with this appetite-stimulating opiate in wheat.

Ignorance of the gliadin effect of wheat is responsible for the idiocy that emits from the mouths of gastroenterologists like Dr. Peter Green of Columbia University who declares:

"We tell people we don't think a gluten-free diet is a very healthy diet . . . Gluten-free substitutes for food with gluten have added fat and sugar. Celiac patients often gain weight and their cholesterol levels go up. The bulk of the world is eating wheat. The bulk of people who are eating this are doing perfectly well unless they have celiac disease."

In the simple minded thinking of the gastroenterology and celiac world, if you don't have celiac disease, you should eat all the wheat you want . . . and never mind about the appetite-stimulating effects of gliadin, not to mention the intestinal disruption and leakiness generated by wheat lectins, or the high blood sugars and insulin of the amylopectin A of wheat, or the new allergies being generated by the new alpha amylases of modern wheat.

Jelly beans and ice cream

What if I said: "Eliminate all wheat from your diet and replace it with all the jelly beans and ice cream you want."

That would be stupid, wouldn't it? Eliminate one rotten thing in diet--modern high-yield, semi-dwarf wheat products that stimulate appetite (via gliadin), send blood sugar through the roof (via amylopectin A), and disrupt the normal intestinal barriers to foreign substances (via the lectin, wheat germ agglutinin)--and replace it with something else that has its own set of problems, in this case sugary foods. How about a few other stupid replacements: Replace your drunken, foul-mouthed binges with wife beating? Replace cigarette smoking with excessive bourbon?

Sugary carbohydrate-rich foods like jelly beans and ice cream are not good for us because:

1) High blood sugar causes endogenous glycation, i.e, glucose modification of long-lived proteins in the body. Glycate the proteins in the lenses of your eyes, you get cataracts. Glycate cartilage proteins in the cartilage of your hips and knees, you get brittle cartilage that erodes and causes arthritis. Glycate structural proteins in your arteries and you get hypertension (stiff arteries) and atherosclerosis. Small LDL particles--the #1 cause of heart disease in the U.S. today--are both triggered by blood sugar rises and are 8-fold more prone to glycation (and thereby oxidation).

2) High blood sugar is inevitably accompanied by high blood insulin. Repetitive surges in insulin lead to <em>insulin resistance</em>, i.e., muscles, liver, and fat cells unresponsive to insulin. This forces your poor tired pancreas to produce even more insulin, which causes even more insulin resistance, and round and round in a vicious cycle. This leads to visceral fat accumulation (Jelly Bean Belly!), which is highly inflammatory, further worsening insulin resistance via various inflammatory mediators like tumor necrosis factor.

3) Sugary foods, i.e., sucrose- or high-fructose corn syrup-sweetened, are sources of fructose, a truly very, very bad sugar that is metabolized via a completely separate pathway from glucose. Fructose is 10-fold more likely to induce glycation of proteins than glucose. It also provokes a (delayed) rise in insulin resistance, accumulation of triglycerides, marked increase in formation of small LDL particles, and delayed postprandial (after-eating) clearance of the lipoprotein byproducts of meals, all of which leads to diabetes, hypertension, and atherosclerosis.

I think we can all agree that replacing wheat with jelly beans and ice cream is not a good solution. And, no, we shouldn't have drunken binges, wife beating, smoking or bourbon to excess. So why does the "gluten-free" community advocate replacing wheat with products made with:

rice starch, tapioca starch, potato starch, and cornstarch?

These powdered starches are among the few foods that increase blood sugar (and thereby provoke glycation and insulin) higher than even the amylopectin A of wheat! For instance, two slices of whole wheat bread typically increase blood sugar in a slender, non-diabetic person to around 170 mg/dl. Two slices of gluten-free, multigrain bread will increase blood sugar typically to 180-190 mg/dl.

The fatal flaw in thinking surrounding gluten-free junk carbohydrates is this: If a food lacks some undesirable ingredient, then it must be good. This is the same fatally flawed thinking that led people to believe, for instance, that Snack Well low-fat cookies were healthy: because they lacked fat. Or processed foods made with hydrogenated oils were healthy because they lacked saturated fat.

So gluten-free foods made with junk carbohydrates are good because they lack gluten? No. Gluten-free foods made with rice starch, tapioca starch, potato starch, and cornstarch are destructive foods that NOBODY should be eating.

This is why the recipes for muffins, cupcakes, cookies, etc. in this blog, the Track Your Plaque website, and the Track Your Plaque Cookbook are wheat- and gluten-free and free of gluten-free junk carbohydrates. And put that bottle of Jim Beam down!

Diet by LDL

Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

So, cut the saturated fat in the diet, cut the overall fat content, and replace them with polyunsaturated oils like safflower, corn, and vegetable oils and increase consumption of whole grains and total and LDL cholesterol show a modest downturn. Thus, diets like the American Heart Association Total Lifestyle Change approach advocate limiting total fat to no more 25 to 35% of calories and saturated fat to no more than 7% of calories.

Orange Cream Cookies

If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

Ingredients:
2 cups almond meal
2 tablespoons coconut flour
1 teaspoon baking soda
½ teaspoon sea salt
¼ cup golden raisins
½ cup chopped pecans
Sweetener equivalent to 1 cup sugar
2 tablespoons finely-grated orange rind
1 large egg
2 tablespoons coconut oil, melted
½ cup whipping cream (or coconut milk)
1 tablespoon vanilla extract

Preheat oven to 350º F.

Combine almond meal, coconut flour, baking soda, salt, raisins, pecans, sweetener and orange zest in bowl and mix.

In separate bowl, whisk egg, then add coconut oil, whipping cream, vanilla extract and mix together. Pour wet mix into dry and blend by hand thoroughly.

Spoon onto parchment paper-lined baking pan (or oiled pan) and flatten with spoon to ½-¾ inch thickness. Bake for 20-25 minutes or until toothpick withdraws dry.

Why are heart attacks still happening?

I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease.

But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.)

Two high-profile deaths from heart attacks occurred this week:

Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain.

Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking.

It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health.

The followers of the Track Your Plaque program who

1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes)
2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction
3) correct the causes

enjoy virtual elimination of risk.

My letter to the Wall Street Journal: It's NOT just about gluten

The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health
All posts by william-davis

Who knows what

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”

“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

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?

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)


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

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

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?”

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

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

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.)