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.

Vitamin D Newsletter-Autism and Vitamin D

Although Dr. John Cannell's most recent Vitamin D Newsletter concerns the connection between autism and vitamin D, and has nothing to do with coronary plaque reversal, this fascinating discussion between a mother of an autistic boy and Dr. Cannell is so enlightening that I thought that it was still worth passing on.

I also feel very deeply for parents with autistic children, who I see struggle with the developmental difficulties their children encounter. (I even have several patients who are parents of 2 or 3 autistic children.)

As always, Dr. Cannell is at the cutting-edge of converting hard scientific information into practical use. You will note several points or questions raised:

1) Dr. Cannell advocates a powdered capsule form of vitamin D. In my experience, most powdered or tablet forms do not work. But some do. He apparently has success with the brand he specifies.

2) Are there vitamin D-receptor (VDR) genotypes that respond differently? Should there be different 25 (OH) vitamin D blood level targets for different VDR genotypes? Nobody knows yet, but it will be an important question to explore in the future.

3) Is heavy metal toxicity, at least in its milder forms, a surrogate for vitamin D deficiency? (Are chelationists unwittingly treating vitamin D deficiency?)

4) If this is a genuine association, and vitamin D replenishment exerts profound neurologic effects in autistic children, does a similar, though less marked effect, hold in non-autistic children? Will children perform better, learn more effectively, etc. with vitamin D supplementation to normal levels?

5) Vitamin A--Is vitamin A with vitamin D good or bad? This one I do not have an answer to. Reading the literature Dr. Cannell cites didn't help much. (Dr. BG--Any comments? Dr. BG is a vitamin A advocate.)


Perhaps, should the association between autism and vitamin D hold, it raises more questions than it settles. But, true to my experience with vitamin D, every day I stumble on some unique, fascinating effect, all beneficial. We continue to learn new lessons about vitamin D and Dr. Cannell's insights as a practicing psychiatrist deeply concerned with vitamin D issues have helped enormously.

(Sorry, but I did not copy the links to the literature Dr. Cannell cites. To obtain the links, go to the original Vitamin D Newsletter.)

The Vitamin D Newsletter
June 2008




This month we feature a remarkable series of letters from a mother of an autistic son who treated her child with vitamin D. It is the first case report in the medical literature suggesting vitamin D has a treatment effect in autism.

First, a brief case report and then a more detailed exchange of emails between the mother and me.

Case Report:

John is a seven-year old boy living in the northeastern U.S. with a long-standing diagnosis of autism. Symptoms include temper tantrums, repetitive self-stimulatory behavior, impaired language, mood swings, fear of being alone, toileting problems, dysbacteriosis, and impaired muscle strength. John spends a lot of time outdoors starting in the spring and his mother noticed a distinct seasonal variation in his symptoms in that he improved in the summer and regressed in the winter. A 25-hydroxy-vitamin D in April of 2008 was 25 ng/ml and obtained after John had begun to play outside. Due to the seasonality of John's symptoms the mother consulted me. I advised the mother to stop all products containing vitamin A including cod liver oil and begin John on 5,000 IU of vitamin D3 per day for two weeks followed by 2,000 IU per day in the form of powdered vitamin D dissolved in juice. Within a week of starting the vitamin D, John's language began to return and he was no longer as fearful of being alone. At the end of two weeks his language showed further improvement, he began to toilet himself, counted to 10 and knew the spelling of his name. After three weeks language continued to improve and some improvements were noted in his dysbacteriosis. After four weeks of vitamin D treatment, the mother noted improvements in muscle strength as well as continued improvements in language. A repeat 25-hydroxy-vitamin D is pending while John continues taking 2,000 IU of vitamin D per day.

Before you read the series of emails between the mother and me, I'd like to caution that this is only a case report of sorts and does not prove a treatment effect. Spontaneous remissions, while rare in autism, have been reported, thus the supplemental vitamin D may have had nothing to do with his improvement. If the response is due to vitamin D, there is no assurance it will prove lasting. I think it unlikely that older autistic children or individuals with severe autism will show these sorts of apparent improvements. Furthermore, autism is a multifactorial disease with strong genetic roots and it is highly unlikely that treatment of vitamin D deficiency in all autistic children will result in similar improvements. Finally, I did not examine this child, and I am relying on the child's mother to report both his condition and his apparent response to vitamin D treatment. However, the mother agreed to speak with the press about her son and allow for independent confirmation of the apparent treatment response.

Below are the emails, edited for brevity, clarity, and confidentiality.



Dear Dr. Cannell:

I am writing because I believe my son John is strongly affected by vitamin D and I need some advice. John is seven and autistic and weighs 50 pounds. We live in the northeastern part of the United States . He starts spending lots of time outside in May and continues until September. Every year, like clockwork, he has the same patterns of behavior and ability. After about six weeks of sun exposure, every July, he begins feeling much better, seems to be comfortable in his skin, does not have as much self-stimulatory behavior, can eat a variety of foods and has language. This past summer, he was using 14-word sentences. By the end of November, he can't even ask you for a cup of juice. He becomes more exclusive, has emotional highs and lows, has tantrums and is easily frustrated.

His 25(OH)D level on April 15th was 25 ng/ml but he had already been going out in the sun so his level must have been lower in the winter. I have had his genetics tested (Nutrigenomic) and he has mutations in his vitamin D receptors:

VDR Bsm/Taq ++
VDR Fok --
VDR Taq ++

My first question, does it sound like the changes in his behaviors and abilities could be caused by lack of vitamin D? Could you elaborate on the time it would take to get adequate amounts of vitamin D to start seeing positive results? For example, even if he starts going out in the sun in May, it's usually not until July that I see positive changes. Then would it take a month or two to go back to being deficient, thus explaining his 'regression' by the time November comes around. Secondly, I am looking at different forms of vitamin D therapy: a vitamin D lamp, vitamin D3 cream, or oral vitamin D. Can you tell me what might be the best form during the winter months?

Thank you very much for your time and attention.

Jane, Boston MA



Dear Jane:

Yes, it is possible your son's autism is related to vitamin D. Such seasonality has been reported before in autism, both in an individual and in autistic children at a summer camp. Although suggestive, such seasonality does not prove a vitamin D connection. Sun exposure, unless it is full body, takes several months to get vitamin D levels up. If sunblock or clothes are worn sun exposure will not get 25(OH)D levels much above 30 ng/ml. As far as the "mutations" you list, they are actually vitamin D receptor (VDR) polymorphisms and not referred to as mutations although all such changes occurred through mutations at some time in the past. VDR polymorphisms are simply the different structures of the vitamin D receptor that different people have and they are widely distributed. A pilot study of actual VDR receptor mutations did not detect VDR mutations in 24 autistic individuals but they did not assess for VDR polymorphisms. However, a highly significant association exists between one VDR polymorphism and larger head size. Mean head circumference is larger in autism.

Yan J, et al. Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases. Neurosci Lett 2005;380(1-2):37-41.

Handoko HY, et al. Polymorphisms in the vitamin D receptor and their associations with risk of schizophrenia and selected anthropometric measures. Am J Hum Biol 2006;18(3):415-7.

Lainhart JE, et al. Head circumference and height in autism: a study by the Collaborative Program of Excellence in Autism. Am J Med Genet A 2006;140(21):2257-74.

Lainhart JE, et al. Macrocephaly in children and adults with autism. J Am Acad Child Adolesc Psychiatry 1997;36(2):282-90.

I emailed the world's foremost expert on VDR polymorphisms asking him about your son's polymorphisms and his reply, quite technical, is below.



Dear John:

I apologize for the delay in getting back to you regarding VDR polymorphisms. Initial studies by Eisman and coworkers many years ago suggested that several of the polymorphs identified above in the VDR gene (Bsm/Tag) correlated strongly with osteoporosis. Despite the hoopla, subsequent analyses by many different investigators did not really confirm these results, i.e. only a very modest (3%) correlation. This spawned multiple studies searching for correlations between VDR polymorph's and cancer, autoimmune disease and so forth. It is fair to say from all of these studies that the correlation is at best weak, and in most cases non-existent. Part of this may be due to the fact that the Bsm and Taq polymorphs are located in VDR gene introns and as a first approximation cannot affect the VDR protein's function. This is not an absolute statement, however, as our work is now showing that regulatory regions that control the VDR's expression are located within introns as well as upstream. Therefore the possibility exists that these polymorphs could affect expression, although we have not found these regions to contain enhancers yet. This is clearly where gene and disease studies are going. The only polymorph that could affect function is the Fok1 site, which we identified many years ago following our initial cloning and structural analysis of the human VDR gene. The presence of this site leads to the expression of a shorter VDR protein (424 aa) that is purported to have a slight increase in transcriptional activity (10%?) vs the large protein (427 aa). The above analysis suggests that this polymorph is absent, leading to production of the larger perhaps less active protein. On a single patient basis, it is really difficult to conclude anything regarding this finding. Indeed, despite large numbers of patients, the VDR polymorph have not really revealed any significant insight. Given the summer correlations, it is probably more likely that the individual is low in vitamin D3 in winter.

Sincerely,

Professor John Doe




Thus, one of your son's polymorphisms may have less functionality but that should be easily overcome by higher vitamin D levels. The first thing to do is stop all vitamin A, multivitamins containing vitamin A, or cod liver oil and start vitamin D. As you will see below, vitamin A antagonizes the action of vitamin D and he should have plenty of vitamin A if he eats colorful vegetables, colorful fruit, eggs and fortified oatmeal. As far as vitamin D, I think the easiest way to give vitamin D is powdered capsules, not a cream. You can open the capsule and put the powder in about anything, such as juice. To buy the capsules, go toBio Tech Pharmacal and buy both a bottle of the 5,000 and the 1,000 IU capsules. He should take one 5,000 IU capsule a day for two weeks then take 2,000 IU per day. After a month, go to the doctor and have another 25-hydroxy-vitamin D blood test. Do not let your doctor order a 1,25-dihydroxy-vitamin D as it will give you and your doctor false information about your son's vitamin D status. The other option is buying a Sperti vitamin D light. Daily use of the light on both sides of his trunk will raise levels fairly quickly but he should still have a 25(OH)D blood test every month to assure his levels rise to the mid level of normal ranges, about 70 ng/ml. Vitamin D is very safe. Your son would have to take more than 10,000 IU a day for more than a year to have any risk of toxicity. If he improves and his level is 50 ng/ml, the next question is would he improve even more if his level was 70 ng/ml? Some lifeguards have levels of 80-100 ng/ml; normal ranges in the labs in the USA are 30 -100 ng/ml (ideal ranges are 50 -100 ng/ml.) If you have any more questions, let me know. I certainly want to know how he is doing.

Sincerely,

John Cannell



Dear Dr. Cannell:

It has been one week on 5,000 IUs of vitamin D3 daily and already we're getting some language back! We haven't had original language since probably around the end of November. The only language we have had in the past five months has been verbal scripting. Today John has already told me "turn off the TV" and "clean up the water". This is all very exciting. Will it last? I will continue to keep you updated on progress and change in behavior. One more thing, all winter long he was afraid to be by himself anywhere. Now he is starting to be able to be in another room or outside by himself.

Thanks so much,

Jane



Dear Jane:

I can't tell you how happy I am for you. I suspect John will continue to improve. Do you have any parent rating scales or does his treating pediatrician have any objective rating scales? If you have before and after rating scales or his treating doctor does then it becomes important to track his progress on an objective measure. Jane, if you are a member of any autism discussion groups, you should post about this, including doses used. If your son's case is typical, then hundreds of thousands of autistic children may be helped with vitamin D.

John Cannell



Dear Dr. Cannell:

It has been two weeks on 5,000 IU per day and I want to inform you that we are having continued success with language. Continued in the sense that it is consistent, it wasn't just a one day fluke. In addition, he is taking himself to the bathroom; this is another thing that goes away in winter months. I usually have to catch him holding it in and then suggest he go, but now he is going completely by himself. In therapy last week, he started drawing again. He drew a bee and then ran around the room buzzing. His toileting is consistent with his therapists, not just mommy. Last night, I asked him to count to 10 for me and he did - quite enthusiastically. Then I said what does J-O-H-N spell? It took him a bit but then he said "John."

Unfortunately, the last scale taken was when he was 3 when he had his first developmental evaluation. But we do track behavior and language on a weekly basis. The forms we fill out give a good indication as to how he is doing.

I belong to a parent forum. It was created by a doctor named Amy Yasko. She's a PhD, a researcher, not a medical doctor. It was through her that I got John's genetics tested. She advocates vitamin D as being very crucial. I will post something on her forum for the parents there. However, if the parents on the forum are following her recommendations, they should be taking it already - 2000 IUs in winter and 1000 IUs in summer is her recommendation. I will post something on the forum to really emphasize how important vitamin D is.

Jane



Dear Jane:

I'm glad the improvements are continuing. I see Dr. Yasko recommends 10,000 IU of vitamin A/day as well as cod liver oil. I strongly disagree. Make sure your son is taking neither vitamin A nor cod liver oil. Rather, make sure he eats colored fruits and vegetables as well as fortified oatmeal. Vitamin A interferes with vitamin D's function, especially at the doses Dr. Yasko recommends.

Vitamin A antagonizes the action of vitamin D. In humans, even the vitamin A in a single serving of liver impairs vitamin D’s rapid intestinal calcium response. Furthermore, the consumption of preformed retinols, even in amounts consumed by many Americans in both multivitamins and cod liver oil appears to be causing low-grade, but widespread, bone toxicity, perhaps through its antagonism of vitamin D. In a recent dietary intake study, Kyungwon et al found high retinol intake completely thwarted vitamin D’s otherwise protective effect on distal colorectal adenoma and they found a clear relationship between vitamin D and vitamin A intakes as the women in the highest quintile of vitamin D intake also ingested almost 10,000 IU of retinols/day. As early as 1933, Hess et al warned about vitamin A consumption, concluding, “as to a requirement of thousands of units of vitamin A daily, the unquestionable answer is that this constitutes therapeutic absurdity, which, happily, will prove to be only a passing fad.”

Rohde CM, Deluca HF. All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats. J Nutr. 2005;135(7):1647-1652.

Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905.

Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;83(2):191-201.

Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL. Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol. 2007;165(10):1178-1186.

Hess AF, Lewis JM, Barenberg LH. Does our dietary require vitamin A supplement? JAMA. 1933;101:657-663.

Unfortunately, Hess’s prophecy of a passing fad proved premature and many Americans continue to consume “absurd” and dangerous quantities of vitamin A. For example, multivitamins, until recently, had small amounts of vitamin D (200 to 400 IU) but high amounts of preformed retinols (5,000 to 10,000 IU). This pales in comparison to a tablespoon of modern cod liver oil, which contains sub-physiological amounts of vitamin D (400 to 1200 IU) but supra-physiological amounts of completely preformed retinols (5,000 to 15,000 IU or in some cases 30,000 IU).

John Cannell



Dear Dr. Cannell:

It has been three weeks and he went from 5,000 IU of vitamin D per day to 2,000 IU per day a week ago. His language is increasing. He's now back to saying the things he wants with some prompting. He also has gut dysbiosis and I'm sure the D is helping with microbes in his gut. He has a lot of problems with his immune system and bacteria and viruses. Also, doesn't vitamin D aid in the production of glutathione? I feel that could be a big part of his increased language.

Jane



Dear Jane:

Yes, abnormal immune responses are associated with both autism and vitamin D deficiency. For example, autistic individuals have immune abnormalities that show a striking similarity to the immune functions affected by vitamin D. Animal evidence indicates some vitamin D deficiency induced brain damage may be malleable, that is, vitamin D may partially reverse the brain damage, if given early enough. These studies offer hope that sunlight or oral vitamin D, especially in young autistic children, may have a treatment effect.

Ashwood P, et al. The immune response in autism: a new frontier for autism research. J Leukoc Biol 2006;80(1):1-15.

Cantorna MT, et al. Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system. Am J Clin Nutr 2004;80(6 Suppl):1717S-20S.

Burne TH, et al. Combined prenatal and chronic postnatal vitamin D deficiency in rats impairs prepulse inhibition of acoustic startle. Physiol Behav 2004;81(4):651-5.

Both the brain and the blood of autistic individuals show evidence of ongoing chronic inflammation and oxidative stress. That is, the disease process is probably increasingly destructive. Further hope for a treatment effect rests in activated vitamin D's powerful anti-inflammatory properties. Its administration reduces production of inflammatory cytokines in the brain, which have consistently been associated with cognitive impairment. Furthermore, activated vitamin D is remarkably neuroprotective by stimulating neurotropin release, reducing toxic cellular calcium levels in the brain, inhibiting the production of nitrous oxide, and by its immunomodulating properties, especially in reducing inflammatory cytokines and by increasing brain glutathione.

Moore ME, Piazza A, McCartney Y, Lynch MA. Evidence that vitamin D3 reverses age-related inflammatory changes in the rat hippocampus. Biochem Soc Trans 2005;33(Pt 4):573-7.

Cohen-Lahav M, Shany S, Tobvin D, Chaimovitz C, Douvdevani A. Vitamin D decreases NFkappaB activity by increasing IkappaBalpha levels. Nephrol Dial Transplant 2006;21(4):889-97

Kalueff AV, Eremin KO, Tuohimaa P. Mechanisms of neuroprotective action of vitamin d(3). Biochemistry (Mosc) 2004;69(7):738-41.

This last function of vitamin D, increasing cellular levels of glutathione, may explain the purported link between heavy metals, oxidative stress, and autism. For example, activated vitamin D reduces iron-induced and zinc-induced oxidative injuries in rat brain. The primary route for the neurotoxicity of most heavy metals is through depletion of glutathione and subsequent generation of reactive oxygen and nitrogen species. Besides its function as a master antioxidant, glutathione acts as a chelating (binding) agent to remove heavy metals. Several studies indicate autistic individuals have difficulty excreting heavy metals, especially mercury. If vitamin D deficient brains are unable to utilize glutathione properly, and thus unable to remove heavy metals, they may be oxidatively damaged by heavy metal loads normal children easily excrete. The amount of activated vitamin D in the brain directly depends on how much vitamin D is made in the skin or put in the mouth.

Garcion E, Wion-Barbot N, Montero-Menei CN, Berger F, Wion D. New clues about vitamin D functions in the nervous system. Trends Endocrinol Metab 2002;13(3):100-5.

Chen KB, Lin AM, Chiu TH. Systemic vitamin D3 attenuated oxidative injuries in the locus coeruleus of rat brain. Ann N Y Acad Sci 2003;993:313-24.

Lin AM, Chen KB, Chao PL. Antioxidative effect of vitamin D3 on zinc-induced oxidative stress in CNS. Ann N Y Acad Sci 2005;1053:319-29.

Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12(10):1161-208

Kern JK, Jones AM. Evidence of toxicity, oxidative stress, and neuronal insult in autism. J Toxicol Environ Health B Crit Rev 2006;9(6):485-99.

Sincerely,

John Cannell



Dear Dr. Cannell:

It has been a month now and John's Improvements are continuing. In the last week, he has been using his muscles more, he goes on the swing outside and lifts his legs and bends in ways that take core muscle strength. This is yet another skill or interest that left and is returning. I will report more next week.
Jane




Conclusion:

It is too early to say vitamin D has a treatment effect in autism. However, a simple risk/benefit analysis suggests that autistic children should be diagnosed and aggressively treated for vitamin D deficiency. If readers want to learn more about vitamin D and autism, they can obtain the entire paper on the link below. Unfortunately, Elsevier charges $31.50 to download it. You can read a similar document for free on the website, where we first published the theory a year ago.

Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9.

http://vitamindcouncil.org/newsletter/2007-may.shtml

In summation, autistic children should be given enough vitamin D to get their 25(OH)D levels up to the mid to high range of normals, that is, 70 ng/ml (175 nmol/L in countries that use the metric system). In the absence of sun exposure, this usually requires long-term administration of about 1,000 IU/day per 20 pounds of body weight with a loading dose of 2,000 IU of vitamin D/day for every 20 pounds of body weight for the first two weeks. As individual variation in response is very high, they should have 25(OH)D blood tests every month until their level has stabilized around 70 ng/ml. They should stop all products containing preformed retinols (vitamin A), especially cod liver oil.

John Cannell, MD
The Vitamin D Council

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. As we are a 501(3)(c) non-profit corporation, dedicated to ending vitamin D deficiency and not making money, the Vitamin D Council does not copyright this newsletter. Please reproduce it and post it on Internet sites. If this newsletter proves useful to a child you know with autism, the Vitamin D Council asks for a donation as we have not been able to secure a grant and our bank account balance is again below $5,000. Send your tax-deductible contributions to:

The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

"Make big money fast with CT scans"

Rather than the headline New Study Could Change Heart Disease Diagnosis And Treatment being run in Utah TV and newspapers, instead it should read:


Make big money fast with CT scans!

Is your bottom line shrinking? Have you fallen on hard economic times? Is competition from other hospitals and providers threatening your financial health?

Then we have a solution: Do a CT coronary angiogram on everybody! Look for disease in people with no symptoms, scare the heck out of them, and voila! Instant need for bypass surgery!

Ka-ching!! That'll be $100,000, please.

Do it again, and again, and again, and your hospital will be quickly in the black in no time!

And, for the savvy marketer, tell the newspapers that you're going to conduct a study to see if this approach works--even before the study gets started! Even if the study pans, you'll come out a winner because you did it in the name of "research"!




Apparently a group of cardiologists at the Intermountain Medical Center and LDS Hospital in Salt Lake City, with the financial assistance of Siemens, a manufacturer of CT scanners, is funding a 1000-patient study of diabetics, all without symptoms of heart disease, half of whom will undergo "screening" CT coronary angiograms (not heart scans) followed by bypass surgery, if "needed". The other half will receive conventional, "aggressive" medical therapy. "Aggressive" means cholesterol treatment, blood pressure control, and blood sugar control (no kidding).

The outcomes of the two groups will be compared after two years.

To understand the absurdity of this study, note that they are proposing what amounts to "prophylactic" bypass surgery, since the participants are without symptoms. Since there are no stress tests, a measurement of flow or functional capacity (exercise tolerance) cannot be factored in. Decisions will be made on the basis of severity of "blockages" in asymptomatic people, a hazardous notion that has never been shown to provide benefit. No doubt: Some diabetics with extensive disease may obtain benefit from screening, but many more will undergo what amounts to unnecessary bypass that provides no benefit. We already know from studies dating back over 20 years to the days of the original CASS (Coronary Artery Surgery Study) that putting asymptomatic people through bypass surgery willy-nilly does not reduce mortality.

Of course, the "aggressive" preventive treatment they propose is more like the least common denominator level of treatment. In fact, I would characterize the "aggressive" preventive treatment as ridiculous. Doing less would be malpractice. Much more could be done, but doing a lot more would pose a real challenge to the bypass arm of the trial.

But the smell of money drives such efforts: More CT angiograms, more hospitalization for bypass surgery. The payoff to the hospitals from this effort is likely to exceed $5 to $10 million, all money that they might not have otherwise seen. The ill-informed people in the local media gush with enthusiasm, the hospital acts like they are at the cutting edge of medical technology, the doctors pose as saviors.

All this time, real preventive efforts go unmentioned. No fish oil (28% reduction in heart attack, 45% reduction in sudden death from heart attack), no genuine diet efforts (i.e., not the diabetes-promoting American Diabetes Association diet), no effort to identify sources of coronary risk beyond LDL cholesterol (low HDL,small LDL,and postprandial or after-eating abnormalities, for instance, are prominent sources of risk in diabetics), no vitamin D. In my view, the preventive arm of the study amounts to doing virtually nothing beyond prescribing statin drugs.

Don't fall for it.

Is DHEA dangerous?

















The Fountain of Youth, Louis Cranach the Younger (1546)




In the Track Your Plaque program, we sometimes use the adrenal hormone, DHEA. It is a fascinating and--surprisingly--an over-the-counter hormone that can be useful and safe when used properly.

DHEA can be useful for:

--Reduction of Lp(a)--Though more effective in females, it can also be useful in males. In the women, DHEA often reduces Lp(a) 15-18%, somewhat less in males. The lower the starting DHEA, the greater the Lp(a) reduction.

--Improved libido--in both men and women. The effect is modest. It's magnified when used with other strategies. Although this is not specifically a goal in the program, it sure helps to get side-benefits like this, rather than unwanted side-effects.

--Increased energy and mood--The boost in mood is, for many, the most perceptible effect: More ambition, more stamina, greater staying power in work and exercise.

--Reduction in abdominal (visceral) fat--A modest effect, but one that, over a long period of use (>6 months) can yield improved insulin responses.


Most commonly, I will suggest DHEA supplementation when blood levels allow. Some people, however, Google "DHEA" and come back horrified that I would suggest such a dangerous supplement.

"I read that it makes women grow mustaches and makes their voices deeper!"

And it does--if you take a lot.

10-15 years ago, when the benefits of DHEA became apparent, some people wanted to believe that DHEA was the fountain of youth. People interested in the anti-aging potential for DHEA figured that, if 50 mg per day made you feel energized and vigorous, what would be the effect of 1000 mg, 2000 mg, or 3000 mg per day? A number of clinical trials were conducted using these doses and, interestingly, depression can lift, men and women increase muscle mass, there is a slight increase in bone density, even pain symptoms from rheumatoid arthritis and lupus may improve. But . . . women grow mustaches, become sexually aggressive, and develop deep voices. Men can become hyperaggressive or overly emotional.

No wonder: Any hormone taken in extraordinary, supraphysiologic doses will exert wacky effects. Imagine taking testosterone or estrogen at 50 times the usual dose.

The doses we use for the above benefits, including Lp(a) reduction, range from 25-100 mg per day; most people do fine with 50 mg. We also adjust doses to starting blood levels. In this dose range, I have never seen any of the above side-effects.

The only side-effects I see at these doses are 1) excessive assertiveness or crabbiness, and 2) insomnia if taken at bedtime.

In my experience, DHEA is a benign hormone, provided it is taken in limited doses and not abused. An occasional female younger than 55 years old will be able to tolerate only 10-20 mg per day before developing the edgy side-effects, but I've never witnessed masculinizing side-effects at these low doses, nor have I ever seen excessive increases in testosterone in men or women. (Women can raise testosterone levels slightly, but almost never enough to exert much effect beyond modestly increased libido.)



Copyright 2008 William Davis, MD

Wheat addiction: 140 lbs lost

Here is detailed comment from a reader who figured out the wheat (and dairy) issue on her own with impressive results.

Though it seems an unpardonable over-simplification of diet, this concept of eliminating wheat-based products (along with obvious unhealthy foods like candy and soda) yields unexpectedly large results, as our reader relates.


Hi Dr. Davis,

Several years ago, chronic untreated asthma infections hospitalized me. I thought it was recurring bronchitis as I'd never had asthma in my life. Killed much of the alveoli... took awhile to de-crap the lungs and regrow the alveoli. Got assigned a cardiologist sort-of by accident while in the hospital for that (couple days of constant heated steroid, stress, a pain + situation combined, elevated my heart rate to 298 for a brief time). When I went to see him, he wrote me a prescription for the Eades' PPLP [Protein Power LifePlan] book.

It's taken awhile, since it's required radical gradual changes in most aspects of my overly Type-A life, but I'm now about 140 lbs lighter, and hopefully much more in the future.

Miraculously, after 10 days on a hard meat-eggs-cheese-veggie-berry approach (which I sadly confess was mostly pepperoni & mozz nuked... I was busy! ;-)), all my medical symptoms disappeared too. Acid reflux, acne, brain-fog, rashes, 'severe asthma', allergies, etc. etc. By trial and error I realized I wrongly attributed that to lowcarbing when it was getting off gluten that actually did it for me. Which since I'm lowcarb also means all the crap my celiac boyfriend can eat, I can't. Lowcarb does many great things for me (just dropping all the bloating and increasing the energy level are awesome), but getting off wheat was critical.

I've since found that a single tablespoon of "milk" in the morning, or something with wheat (say a tortilla), will make me ravenous *specifically for milk and wheat* all day. Conversely, I can be eating lowcarb and then eat total junk--but something without gluten--and not have it bother me much at all. But one pumpernickel slice at Outback and I am DOOMED. It doesn't always happen that instant; will-power has some sway; but the odds of my making a 'poor decision that leads to cascade failure and totally abandoning my eating plan' in the next 48 hours is astronomically higher if milk or wheat were involved. Oddly, cheese does not seem to affect me this way.

When I was younger (I'm 42 now) I had to stop drinking milk. If I drank some I wanted more. If I drank more I needed more. If I drank more, that was it: I'd be stumbling to the kitchen in the dark at 3am, drinking out of the carton, falling gasping against the refrigerator after several long gulps, like a heroin addict who just got a fix. I finally realized that since I'd lived on a ton of milk my whole life, maybe this was a milk problem; so I usually stayed away from it. So then it turned out wheat/gluten were an issue too. Which made me realize how much of my life was filled with not-eating most of the time (very busy, workaholic, but very sedentary), but when I did eat, ingesting amazing amounts of wheat products. I'm astounded that my whole life I mostly ate things I am apparently intolerant to "or something." Sometimes I wonder how much different even my brain would be if it'd been different.

This might contribute to my ending up weighing 500# at one point. The only amazing thing is that I didn't get a disease. (Well I did--obesity--but I mean any others.) I'm from a family of people who are mostly fat, mostly alcoholic, and mostly dead of cancer. I'm just fat, worse than the others but otherwise seemingly ok. Now I'm starting to think that maybe my whole family may have some 'issue' with the primary foods of our culture.

I tell friends that my horrible chronic acid reflux was solved merely by getting off gluten. They nearly all say, "I could never give up bread!" (Isn't it funny, you never hear people say, "Oh man, I could never give up broccoli!") I tried to convince one young friend to try it; her doctor told her eating more protein and fat was unhealthy, and gave her a prescription (this is lifetime--it doesn't cure it, merely treats the symptom) to a drug to help with acid reflux. I said you're kidding me, you think taking a drug the rest of your life is healthier than trading your pasta for a steak?? Go figure.

I still haven't figured out the milk connection (or why I seem ok with cheese for some reason; maybe there is a dosage-difference, or the sugar combined with it has some effect), but I think it's pretty clear that dropping milk and wheat has very radically changed my life for the better. I may actually live, which being a single mom to an awesome 11 year old girl, is a good thing.

Best,
P.

Diet: Don't be angry, be GRATEFUL


Given the confusion over what constitutes the "ideal" diet, a discussion that has been hotly debated for decades, some people become very angry that we still don't agree on what is truly healthy.

"Why should I even try if the experts don't agree? They say something is bad one day, then say it's okay the next!"

But that's a short-sighted half-truth born of frustration. We have certainly zigzagged in our understanding of diet over the years. The grand national experiment in low-fat eating, for instance, clearly failed to improve our health. In fact, the opposite occurred: The largest epidemic of obesity and diabetes in world history. You could get angry from this failed experiment . . . or you could learn from it, take what lessons we can and improve on it.

Step back for a moment and consider: In what other age could we even have this discussion?

If we lived in a world where you were hungry, your children were hungry, and you didn't know where the day's food was to be found, we would have no need whatsoever for this conversation: You would take whatever you could find, kill, or steal.

Say you woke up this morning and your cabinets and refrigerator were empty. The stores were far away or non-existent. You and your family would have to improvise, to forage or hunt your day's food. It would require hours. You wouldn't fuss about glycemic index, or saturated fat, or whether or not sugar or wheat was present. You would just eat whatever you could get your hands on. When caloric deprivation threatens, we take what is available.

But we live in a world of plenty--of enormous excess--that allows us choices. It is a world that encourages eating more than is required for existence, a world tailored more to indulgence than to simple satiety or sustenance. That's when distinctions among food types and quality make a difference. But it is a dilemma born of riches.

Starvation and caloric deprivation would settle the argument for us very quickly. It doesn't mean that we shouldn't continue to debate the finer points of diet. But don't do it with anger or frustration. Do it GRATEFULLY, recognizing that we are lucky to be able to have such a conversation in the first place.


Image courtesy Food and Agriculture Organization of the United Nations.

HDL for Dummies

I frequently peruse conventional health websites to keep track of their message. One painfully conventional (read "drug company-supported") website that echoes the standard advice on heart disease and heart health is Everyday Health .

Since I subscribe to the newsletters for many conventional sites, I received an e-mail that took me to this Q & A about HDL cholesterol:

Q: I'm 36 years old and my good cholesterol is too low. What can I do?
– Nilsa, Florida

Dr. Lori Mosca of New York-Presbyterian Hospital responds:

A: A woman's HDL goal should be greater than 50 mg/dL (greater than 40 mg/dL in men). You can raise your HDL levels by eating a diet low in saturated fat and trans fat but high in monounsaturated fats. Lose weight if you need to and get at least 30 minutes of moderate-intensity exercise on a minimum of four days per week. If you smoke, quit. Despite positive lifestyle changes, though, some individuals may still be candidates for HDL-raising drug therapy because they are at increased risk for cardiovascular disease. Discuss your options with your health care provider.


Are you satisified with that answer? I certainly am not.

First of all, is this something you've never heard before? "Eat right, exercise, cut your unhealthy fats." Then why do people who follow this sort of conventional advice often still fail? Is the next step always medication?

Here's the part that Dr. Mosca and other conventional, drug-minded "authorities" have left out:

To raise HDL powerfully--not to 40 mg/dl for males or 50 mg/dl for females, but to 60, 70 or 80 mg/dl--think about the following strategies:

--Eliminate wheat and cornstarch products. I have droned on endlessly about this concept, but it is enormously effective. While the weight loss that inevitably follows elimination of these foods adds to the HDL-raising effect, there is also an independent effect, as well.

--Fish oil--The omega-3 fatty acids in fish oil reduce triglycerides. Triglycerides accelerate the destruction of HDL. Remove triglycerides, HDL goes up. (Though krill oil may share, even surpass this effect, we need more data than the single manufacturer-sponsored study.) Of course, this requires real doses, not the namby-pamby doses you often read about.

--Vitamin D--Achieving normal levels of 25(OH) vitamin D raises HDL with power I have never witnessed from any other strategy before, barring weight loss of 30+ lbs. Readers of the Heart Scan Blog know that just taking vitamin D is not enough. Verification with blood levels is an absolute necessity, particularly if raising HDL maximally is among your goals.

--Adding back saturated fat. I say "adding back" since most of us (including myself) went too far down the "saturated fat is bad" path over the past few years. While I do not advocate a carte blanche approach to saturated fat, I believe that adding back eggs (preferably free-range and/or omega-3 rich), lean meats, and hard cheeses is a good idea. The saturated fat in these foods raise HDL 5 or more mg/dl.

--Dark chocolate--Or other cocoa prepartions. What a cool way to raise HDL! Reach for the lowest-sugar, highest cocoa preparations.

--Alcoholic beverages--I am partial to the red wine/flavonoid-rich concept, being a wine drinker. Although all alcoholic beverages raise HDL due to the ethanol content, for benefits beyond alcohol (as well as to avoid wheat-based drinks like beer), I do believe that the bulk of data argue for flavonoid-rich red wines from southern France, Italy, and California.

--Achieve ideal weight--The toughest of all. But eliminating wheat and cornstarch makes it far easier.


Follow the conventional advice of those like Dr. Lori Mosca, and the majority of people will fail. ("It just so happens that I have a prescription drug just for that purpose!")

Buck the conventional advice, adopt strategies that won't be found in the drug ads, nor be provided by the conventionally-thinking, and you can succeed to heights you never thought possible.


Copyright 2008 William Davis, MD

"I gained 30 lbs from one cracker"


Let me tell you a story, a tale of a woman who gained 30 lbs by eating one cracker.

At age 50, Claire's health was a disaster. Her initial lipoprotein patterns were a mess, including HDL 36 mg/dl, triglycerides 297 mg/dl, blood sugar 122 mg/dl (pre-diabetic range), blood pressure 155/99. Small LDL comprised over 90% of all LDL particles.

At 5 feet 3 inches, she weighed 210 lbs--90 lbs over her ideal weight. Her face was flushed and red, her eyes swollen and weighted down with bags, her eyes dull. While interested in hearing about how to improve her health, I would hardly call her enthusiastic.

We talked about how removing wheat products entirely from her diet could result in weight loss--enormous weight loss--yet with reduced appetite, increased energy, less daytime sleepiness and fogginess, improved sleep quality. Removing wheat would also allow substantial correction of her lipoprotein patterns with minimal medication.

At first, she seemed confused by this advice. After all, it ran directly opposite to what she'd been told by her family doctor, not to mention the advice from TV, food ads, and food packages.

To my surprise, Claire did it. She didn't return to the office for another 5 months. But she came in, a big beaming smile on her face.

Even at 167 lbs--still overweight--Claire looked great. She glowed. She'd already dropped nearly 2 1/2 inches from her waist. She felt lighter on her feet, discovered energy she thought she'd lost 10 years earlier. Her blood results matched, with dramatic shifts in each and every pattern.

I quizzed Claire on her diet, and she had indeed made substantial changes. In addition to eliminating all foods made of wheat flour, she also eliminated foods made with cornstarch, rice flour, snacks, and other sweets. She ate her fill of vegetables, fruits, raw nuts, lean meats, and healthy oils. She was less hungry while eating less. Even her husband, skeptical at first, joined Claire after the first two months and her initial 20 lbs of weight loss. He, too, was well on his way to dropping to ideal weight.

But a dinner party invitation came. In the few that Claire and her husband had gone to over the few months, she had religiously stuck to her program, choosing cheese, pickles, olives, vegetables that she dipped, but avoided the pretzels, breads, Doritos, potato chips, and others.

This time, a tray of whole wheat crackers was laid on the buffet table, covered with some sort of sweetened cheese. She had just one. She savored the taste that she'd missed. "Maybe one more. I'll be extra good this weekend,'" she told herself.

Now Claire was hungry. The bruschetta covered with tomatoes and mozzarella looked awfully good. "It's got some good things on it, too!" she thought. She had three.

The floodgates opened. I saw Claire three months later, weighing just shy of 200 lbs. "I almost cancelled this appointment," she whispered quietly, tears at the corner of her eyes. "I don't know what happened. I just lost control. After losing all that weight and feeling so good, I blew it!"

I've seen it before: Fabulous success eliminating the foods that created the situation--the insatiable appetite, the endless cycle of hunger, brief satiety, the rolling, rumbling hunger--followed by temptation, then disaster. The weight lost comes right back.

It's experiences like Claire's that have absolutely, positively convinced me: Wheat products are addictive. It's not true for everybody, but it's true for many people, certainly most people who have weight struggles. It triggers some sort of appetite button, a signal to eat more . . . and more, and more. Keep it up long enough, and you have drops in HDL, increases in triglycerides, upward jumps in blood sugar and blood pressure, diabetes, etc. It doesn't matter if it's whole grain, 7-grain, or 12-grain. Yes, the whole grains contain more fiber and more B vitamins. But they all share one characteristic: They trigger a desire for more.

So that's the story of how one whole wheat cracker caused one woman to gain 30 lbs.


Next week's story:

California woman claims: My children are aliens!


Just kidding.


Copyright 2008 William Davis, MD

Wheat-free is not gluten-free

Eliminate wheat from your diet and wonderful things happen:

--Lose 15-20 lbs, sometimes in the first 1-3 months. (More or less, depending on your prior dietary habits, weight, age, etc.)
--HDL cholesterol goes up, triglycerides go down
--Blood sugar drops
--Small LDL is reduced
--C-reactive protein is reduced
--Pre-diabetics often convert to non-diabetics
--Diabetics gain far better control over blood glucose. Some even become non-diabetic (as long as they maintain the wheat-free, low-glycemic index diet and weight control).
--You feel better: Less mental fogginess, more energy, better sleep.
--Appetite shrinks dramatically.


(Many diet programs makes lots of money promising similar results. Prescription medications like the pre-diabetes drugs, Actos and Avandia, and the fibrates, Tricor and Lopid, nearly--nearly--reproduce the effects of eliminating wheat. Of course, these medications do not lead to weight loss or make you feel better. In fact, Actos and Avandia usually trigger a weight gain of 8 lbs in the first year of use.)


All of these wonderful effects develop with elimination of wheat. . . unless you confuse wheat-free with gluten-free. There's a difference.

Remove wheat from your diet, but discover the world of gluten-free products made for people with celiac disease, or gluten enteropathy, and you can regain the weight and recreate many of the phenomena associated with wheat. I've talked about this in past, but it trips up so many people that it's worth talking about again.

The concept that I am advocating is really low-glycemic index (or low glycemic load, actually). Foods that trigger a substantial rise in blood sugar, whether immediate (like whole wheat crackers) or delayed (like whole wheat pasta) are the culprits. The same effects develop with candy, cookies, fruit drinks, pizza, chips, table sugar, and other junk foods.

However, I pick on wheat specifically because it so dominates the American diet. It has grown to fill so many processed food products. It is also a food ingredient that is falsely advertised as healthy. In reality, pretzels, whole wheat crackers, whole grain bread, high-fiber cereals, etc. exert the same effect on blood sugar as candy or white table sugar. They also generate all the "downstream" phenomena listed above.

But wheat is hardly the only food that makes us fat, diabetic, and unhealthy. This is true for foods made with cornstarch (taco shells, cornbread, tortillas, chips, breakfast cereals); rice flour, puffed rice, and polished rice; and potatoes, particularly pulverized potato starch (potato chips). There are others.

These are the gluten-free products that are marketed to the gluten enteropathy (celiac disease) market. Yes, you can make muffins with cornstarch and no wheat gluten, but is it good for you?

No. It is nearly as bad as wheat. It can still skyrocket blood sugar, drop HDL, raise triglycerides, create small LDL, heighten inflammation, etc.

Ground flaxseed, oat bran, barley, quinoa, are some of the alternatives that do not create these effects. But not the majority of gluten-free products on the market.




Ingredients: Potato starch, rice flour, modified corn starch, olive oil, yeast, vegetable protein(lupine), corn syrup, sugar, salt, hydroxypropyl methylcellulose, sodium bicarbonate, ammonium bicarbonate, diacetyltataric acid esters of mono- and diglycerides of edible fats, natural flavor.

". . . only naturally gluten-free and wheat-free ingredients and adhere to the strictest quality processes, testing every batch for gluten using the ELISA assay."

NUTRITION FACTS
Serving Size 7 bread sticks (31g)
Servings per container 5

Calories 120 Calories from fat 25
Amount per serving
Total Fat 2.5g
Saturated Fat 0.5g
Trans Fat 0g
Cholesterol 0mg
Sodium 310mg
Total Carb 24g
Dietary Fiber 1g
Sugars less than 1g
Protein less than 1g

Death to chelation?


Does chelation work?

It's a question I get asked fairly frequently. Although I have never performed chelation, IV or oral, and therefore have no direct experience, my concerns for this purported therapy have included:

1) The concept of extracting calcium from atherosclerotic plaque by removing it first from the blood is absurd. Early chelationists believed that this was the means by which EDTA might reverse coronary atherosclerosis. However, removing calcium from blood would more likely lead to osteoporosis or calcium extraction from bone, since bone is a more ready repository for calcium. Blood calcium levels are also tightly and narrowly controlled; any significant reduction in calcium ("hypocalcemia") can be life-threatening. And, indeed, there have been deaths from hypocalcemia in people receiving chelation.

More recently, chelationists have argued that removal of heavy metals like lead and mercury are responsible for the purported benefits of chelation. And, indeed, blood levels of these heavy metals can be reduced by chelation. That alone may be a benefit. But to then make the leap to say that it also regresses atherosclerotic plaque by the same mechanism has no basis in science.

2) Practitioners associated with chelation tend to be shady. I have seen homeopathic therapies (among THE most ridiculous of concepts), "energy balance" therapies, desiccated organ extracts ("applied kinesiology"), and a variety of other fringe treatments offered by practitioners offering chelation. This doesn't necessarily mean, of course, that chelation is also fringe or suspect, but it tends to be offered by practitioners who engage in generally unscientific, unfounded practices.


The few people I've seen go through multiple courses of chelation (usually 30 or so infusions) have shown no impact on heart scan scores or any other measure of heart disease.

In response to the many questions I receive on chelation, I had been answering that, if we would simply wait for the publication of the NIH-sponsored trial of IV chelation therapy, perhaps we'd know once and for all.

However, in a lengthy criticism, four expert authors argue that the TACT trial to assess chelation study is doomed to failure for an entire list of reasons and should therefore be abandoned. The discussion is available on Medscape Cardiology. (Free sign-in required.)



Why the NIH Trial to Assess Chelation Therapy (TACT) Should Be Abandoned
We investigated the social and the scientific histories of chelation therapy beginning in the 1950s. We examined TACT protocols and consent forms, which, in response to Freedom of Information Act (FOIA) requests, the NIH provided to us with curious redactions. We examined the existing RCTs and the numerous case series cited by the TACT protocols. We examined evidence for risks, including information that is not in the standard medical literature. We examined various hypotheses that advocates have offered to explain how chelation "works."

We present our findings in 4 parts. First, we provide a brief history of the use of disodium EDTA as a treatment for CAD. Next, we describe the origin and nature of the TACT. Next, we discuss the evidence for chelation as a treatment for CAD and for atherosclerosis in general, and place it in the context of other proposed treatments that have been ineffective after an initial period of enthusiasm. Finally, we discuss the risks. For each topic, we contrast our findings with relevant statements in the TACT literature, to the extent that such statements exist.



Among the highlights:

--Since the mid-1970s, court documents and newspapers have reported at least 30 deaths associated with IV disodium EDTA, most of it administered by ACAM members.

--Early chelation investigators had chosen the disodium salt of EDTA, reasoning that if it could remove calcium from atherosclerotic plaques, it might shrink them. That notion was soon demonstrated to be invalid. It has largely been replaced by a "toxic heavy metals" antioxidant hypothesis, which is based on the potential for metal ions to produce free radical damage. Chelationists now cite "removing heavy metals" as the basis for their claim that chelation is effective for approximately 70 conditions, ranging from schizophrenia and autism to cancer. This provides them with numerous reasons to ignore any trial that finds chelation ineffective for CAD.

--Biochemical literature, either not cited or misrepresented in the TACT protocols, has demonstrated that the heavy metals hypothesis is implausible. Antithetically, it also demonstrates that the chelation mixture used in the TACT has pro-oxidant effects in vitro.

--In our opinion, TACT literature -- including 2 versions of the protocol, the consent form, information posted on the NCCAM Web site, and 2 editorials co-authored by the PI -- has misrepresented chelation, its risks, and the facts of the study. It has exaggerated the value of supportive case series, not only by ignoring evidence of bias and incompetence, but by misrepresenting citations and reporting erroneous data. It has minimized the dangers, both by understatements and by omissions of specific, published complications. It has not acknowledged the deaths mentioned above. It has repeatedly conflated disodium EDTA and a different drug, calcium-sodium EDTA.

--The TACT includes nearly 100 "chelation site" co-investigators who, in our opinion, are unsuitable to care for human subjects or to report trial data. Most espouse implausible health claims while denigrating proven methods; several have been disciplined, for substandard practices, by state medical boards; several have been involved in insurance fraud; at least 3 are convicted felons. Several were members of the ACAM or GLACM IRBs mentioned above. Few appear to have real expertise, required by TACT literature, in treating patients with CAD or in conducting clinical trials. Most continue to promote chelation while the TACT is in progress, contrary to good science, to human studies ethics, and to US Federal Code.


While the criticism itself does not prove the point one way or another, as a clinical trial should, anyone contemplating chelation therapy would be well-advised to read the document first. Another reference: EDTA chelation therapy for cardiovascular disease: a systematic review.


The authors of the exhaustive discussion are:
Kimball C. Atwood IV, MD, Anesthesiologist, Newton-Wellesley Hospital, Newton, Massachusetts; Assistant Clinical Professor, Tufts University School of Medicine, Boston, Massachusetts; Associate Editor, Scientific Review of Alternative Medicine
Author's email: katwood@partners.org

Elizabeth Woeckner, AB, MA, President, CIRCARE (Citizens for Responsible Care and Research), Columbia, Maryland

Robert S. Baratz, MD, DDS, PhD, Medical Director, South Shore Health Center, Inc., Braintree, Massachusetts; Assistant Clinical Professor of Medicine, Boston University School of Medicine, Boston, Massachusetts; President, National Council Against Health Fraud, Inc.

Wallace I. Sampson, MD, Clinical Professor of Medicine (Emeritus), Stanford University, Stanford, California; Senior Attending Physician and formerly Chief of Medical Oncology, Santa Clara Valley Medical Center, San Jose, California; Editor-in-Chief, Scientific Review of Alternative Medicine



The authors provided the following disclosures:


Disclosure: Kimball C. Atwood IV, MD, has disclosed no relevant financial relationships in addition to his employment.

Disclosure: Elizabeth Woeckner, AB, MA, has disclosed that she has received compensation for consulting in civil litigation and professional disciplinary actions.

Disclosure: Robert S. Baratz, MD, DDS, PhD, has disclosed that he has been retained by state licensing boards, the Office of the US Attorney, and plaintiff counsel as an expert in disciplinary proceedings and litigation with regard to chelation therapy and associated matters. He is compensated only for his time and has no commercial interest in the outcome of the proceedings or litigation.

Disclosure: Wallace I. Sampson, MD, has disclosed no relevant financial relationships in addition to his employment.

American Diabetes Association


These are actual quotes from the American Diabetes Association website:


Myth #2 (from list of Diabetes Myths): People with diabetes can't eat sweets or chocolate.
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more “off limits” to people with diabetes, than they are to people without diabetes.



Myth #5: If you have diabetes, you should only eat small amounts of starchy foods, such as bread, potatoes and pasta.
Starchy foods are part of a healthy meal plan. What is important is the portion size. Whole grain breads, cereals, pasta, rice and starchy vegetables like potatoes, yams, peas and corn can be included in your meals and snacks. The key is portions. For most people with diabetes, having 3-4 servings of carbohydrate-containing foods is about right. Whole grain starchy foods are also a good source of fiber, which helps keep your gut healthy.





How can I have sweets and still keep my blood glucose on target?
The key to keeping your blood glucose on target is to substitute small portions of sweets for other carb-containing foods in your meals and snacks. Carb-containing foods include bread, tortillas, rice, crackers, cereal, fruit, juice, milk, yogurt, potatoes, corn, and peas. For many people, having about 45 to 60 grams at meals is about right. Serving sizes make a difference. To include sweets in your meal, you can cut back on the other carb foods at the same meal.

For example, you’d like to have cookies with your lunch. Your lunch is a turkey sandwich with two slices of bread. Your first step is to identify the carb foods in your meal. Bread is a carb. You decide to swap two slices of bread for two slices of low-calorie bread and have the cookies -- it’s an even trade. Your total amount of carbohydrate remains the same for the meal.



Can I eat foods with sugar in them?
For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.


Or take a look at the recipes for breads, muffins, cakes, pies, cookies, and pizza.


My point? As I often say, while the "official" organizations like the American Diabetes Association, the American heart Association, and the USDA dominate the message provided to mainstream Americans, to those of us who know better, they have become irrelevant. You can see how obviously boneheaded their advice is. I'd go so far as to say that, if you want diabetes, follow the American Diabetes Association diet. If you have diabetes, and you'd like to accelerate complications like kidney disease, heart disease, and neuropathy, then follow the American Diabetes Association diet.

I'm going to bet that American Diabetes Association sponsors like Lilly, Novo Nordisk, Merck, Pfizer, Abbott ($1 million or more annual contributions) and Cadbury Schweppes (3-year, multi-million dollar support for Weight Loss Matters program) will continue to charge full-speed ahead to maintain the status quo. Cadbury Schweppes are the proud makers of Dr. Pepper, Hawaiian Punch, Snapple, Motts' Apple Juice, and Hires Root Beer--you know, the foods and drinks that you can have as long as you adjust your insulin dose or talk to your doctor about adjusting your diabetes medications. And if you gain, say, 30 or 40 lbs eating these foods. . . well, we've got a treatment for that. Merck's Januvia , for instance, can help you out for only about $200 a month!

Looking at the facts this way, and it seems like some cheap conspiracy theory: They're all out to get us. Dispense information that virtually guarantees propagation of the disease, and all your friends and cronies profit. I don't know if it is or it isn't, but it sure smells like it sometimes.