Vitamin D and autism

This has nothing to do with coronary plaque reversal, nor directly with the Track Your Plaque program, but I found Dr. John Cannell's discussion about the possible relationship between vitamin D and autism so compelling that I thought I just had to pass it on.

So, below are Dr. Cannell's latest thoughts. He takes some criticisms along with praise. I think we owe him a lot for continuing to doggedly promote the benefits of vitamin D.




Vitamin D Newsletter


August, 2007



Dear Dr. Cannell:

I saw an article from a Toronto newspaper about autism and vitamin D. I am currently searching for a vitamin D specialist in the Washington D.C. area to perform a medical work up on my daughter to look for vitamin D-related disorders. The reason I am in search of a vitamin D specialist is that I believe I have stumbled upon a complex relationship in my daughter involving her foot pain, vitamin D, and her autism.

In April 2006, a few weeks after my 3-year-old profoundly autistic daughter began refusing her daily PediaSure drink, she began having excruciating foot spasms lasting from 10-30 minutes at a time, several times a week. She would throw herself on the floor, curl her toes, slam her heels against the floor, and rub the tops of her feet against the carpet, all while screaming the entire time. These were horrible for her to endure, and horrible for my wife and myself to watch. This went on for a year.

From what I read, the symptom was perhaps like foot spasms associated with carpopedal syndrome or tetany. But her blood work did not support that at all. Calcium level was normal (10.2 mg/dL); 25-Hydroxy-vitamin D low (23.5 ng/ml); 1,25 dihydroxy-vitamin D normal (24.7). Despite some vitamin D deficiency, I was assured by medical professionals that nothing supported a vitamin D cause of these particular spasms, so vitamin D was dismissed. Because her calcium level was normal, they told me she did not have tetany, and vitamin D could not be the cause of the pain.

All medical consultants were stymied. I made another research effort and found a 2003 article on WebMD that stated vitamin D has been found to have some link to basic, unexplained muscle and bone pain. By chance, vitamin D was the next supplement we had at home to begin giving my daughter to treat her autism. So, in April 2007 we began giving my 4 year-old profoundly autistic daughter Vitamin D supplements. Her foot spasms which had plagued her for a year diminished within days and disappeared within three weeks. She has not had a spasm in over two months.

In addition, we noted clear improvements in her autistic condition which appear to be from the vitamin D supplements. Eye contact went from zero to fantastic. Her vocalizations increased markedly (still only babbling; she remains completely nonverbal). She appears even happier than previously (she has always been a somewhat happy child). (Please note that my wife and I have tried many dietary supplements over the past 1.5 years guided by a doctor and dietician who both specialize in autism. We honestly state that this is the only thing that has ever had a positive effect on my daughter. We have seen nothing else work.)

My daughter and vitamin D have a complicated relationship. By all counts, looking at her lab work and general condition, vitamin D should have played no role in those excruciating foot fits. And yet it is apparently exactly what is involved in them. And, my wife and I believe at the same time her autistic condition has improved from the vitamin D. The foot fits and her autism appear linked; it was not just a coincidence that this autistic child has those mysterious foot spasms, and the link appears to be vitamin D.

And so I wonder if this is just the tip of the iceberg, if perhaps there is more to know about my child's relationship with vitamin D and what that might mean for her autism. Does she have a specific vitamin D-related disorder? If so, might direct treatment of it also improve her autism further? These are the questions I would like to pose to a vitamin D specialist who could perform a medical work up on my daughter. Please let me know if you know of anyone in the Northern Virginia/Washington DC area. Also, where is the best place to get vitamin D? Thank you for your time.

Sincerely,
Paul, Washington, D.C.




Dear Paul:

I know of no such specialist in the Washington area, indeed no vitamin D/autism expert exists in the world. As far as a specific "vitamin D disorder," linking her spasms, autism, and vitamin D, the world's English language medical literature contains no description of such a disorder. From your daughter's case, it sounds as if PediaSure was her only regular source of vitamin D. If so, her spasms began two weeks after stopping the small amount of vitamin D contained in PediaSure. The spasms continued for a year, ending a few days after you started giving her vitamin D again, this time in the form of a supplement. Several weeks after restarting vitamin D, both you and your wife noticed an improvement in her autism. To my knowledge, this "case report" - your daughter's - is the first ever published.

As no medical literature has ever been published on any of this, all you can do is give her enough vitamin D to get her 25-hydroxy-vitamin D, known as 25(OH)D, into high normal ranges and then wait and hope. Vitamin D's extraordinary mass-action pharmacology implies that simply providing more substrate ([25(OH)D] will help children with low enzyme activity produce more activated vitamin D (calcitriol) in their brains. The vitamin D theory of autism is not simply that vitamin D deficiency in gestation or early childhood causes the disorder. Instead, the theory holds that a quantitative or qualitative abnormality exists in the enzyme system that activates vitamin D.

It could as simple as the normal variation in the enzyme, an enzyme whose activity would vary in a normal or Gaussian distribution, much like height. Some people are tall, some are short, most are in the middle. The same may be true of the enzyme that forms activated vitamin D (calcitriol), some children have a lot of enzyme and some only a little; most are in the middle. As the substrate [25(OH)D] the enzyme metabolizes fell over the last 20 years with sun-avoidance, more and more children on the low end of the enzyme curve are effected by marginally low 25(OH)D levels, explaining both its genetic basis and exploding incidence.

At this point, all your daughter needs is a physician willing to periodically measure her 25(OH)D. Then you can safely supplement your daughter with doses higher than the current Upper Limit for children (2,000 IU/day). You did not tell me your daughter's weight but, assuming she weighs about 30 pounds, even without 25(OH)D blood tests, you can safely give her 50 mcg/day which is 2,000 IU per day. In fact, the U.S. government says this dose is safe for children over the age of one. Life Extension Foundation sells 250 of the 1,000 IU capsules for about ten bucks with powdered vitamin D inside. The powder is tasteless and dissolves easily in juice. Bio Tech Pharmacal, of Fayetteville, Arkansas, told me they were going to be making a 1,000 IU capsule. Or you can get 1,000 IU capsules in a pharmacy or at Costco and crush them. A Canadian firm is now making vitamin D liquid, called Ddrops, with 1,000 IU per drop, but their mail order web site is not yet easily accessed. Beware of cod liver oil; do not use it because vitamin A inhibits the actions of activated vitamin D, and due to the potential for low-grade vitamin A toxicity.

Remember, more and more researchers now believe autism is a progressive, inflammatory, disorder. That is, the inflammation probably progressively destroys brain tissue as the child ages. As I said in my recent paper, I think there is a chance that vitamin D may have a treatment effect in young autistic children if given in adequate doses, due to its anti-inflammatory properties, and its ability to upregulate glutathione, the master antioxidant that also chelates (binds) and then helps excrete heavy metals like mercury. Unfortunately, I see no way, even if the vitamin D/autism theory turns out to be true, that vitamin D can regenerate brain tissue. However, if it stops the inflammation, and cell death, the brain could then begin to develop and learn. These are big ifs. However, you have nothing to lose by trying, the worst that will happen is that it will not help and vitamin D will be added to the long list of false-hope treatments.

Actually, there is a worse possibility. Say the parents of a three-year-old autistic child decide today that vitamin D is nonsense, another false hope, and that I'm a quack. They decide not to give vitamin D supplement their autistic child, who is probably - like your child - vitamin D deficient. Then, it turns out five years from now that scientific evidence shows vitamin D does indeed help. By that time, the child will be eight and will have suffered additional, irreparable, brain damage. In my mind, that is more tragic than another false hope.



Dear Dr. Cannell:

After that article appeared in the Toronto paper, I started my four-year-old son on 1,000 IU of vitamin D two weeks ago. So far the only thing I noticed is that after about ten days, he didn't seem so miserable. The thing that has always broken my heart is that look of sadness and suffering on his face. After about two weeks of vitamin D, I noticed he seemed less miserable. I wouldn't say he looks happy now but that look of misery seems to be gone. Will it come back? I'm not sure I can take it if it comes back. What else might happen? Also, last summer we noticed he seemed to get better, but then he got worse in the fall. We never thought about it until we read about vitamin D.

Susan, Toronto, Canada




Dear Susan:

I don't know. I think all parents have had their heart pierced by that look at one time or another. I would advise increasing the dose to 2,000 IU per day, making sure it is cholecalciferol and not ergocalciferol, and having your doctor order a 25(OH)D every two months to see if he needs higher doses. You want to get his blood level up to between 50 ng/ml and 80 ng/ml (In many countries outside of the USA, that would be reported as between 125 and 200 nmol/L.) and keep it there, summer and winter, and that may take more than 2,000 IU/day in the winter. If vitamin D has a treatment effect, it will take many months to see its full effect. As you noted, if the theory is correct, autistic children who spend time outdoors in the summer should show some seasonal improvements - if they don't wear sunblock and they expose enough of their skin to generate significant amounts of vitamin D.



Dear Dr. Cannell:

I resent you calling autism a tragedy. My son is not a tragedy and I'm glad he was born and is in our lives. He is our joy. Autism is not a tragedy.

Emma, London, England.





Dear Emma:

I'm glad he is your joy and I believe you. I'm new to the autism field and was not aware how much thought and speech control exists in the discussion of the disease. Nevertheless, I have a few politically incorrect questions. If autism is a joy, I assume you would like other parents to have an autistic child? If autism is such a joy, why is there a huge industry forming to prevent and treat it? At the risk of sounding insensitive - apparently one of the most serious charges leveled in the autism debate - autism is a tragedy. As I pointed out in my paper, research shows that having an autistic child, puts the family under more emotional stress than having a child with a fatal illness.



Dear Dr. Cannell:

Who are you to write an article on autism? You didn't even publish it in a medical journal. You are not with a university. You have not published very much. You have no expertise on autism. No autism experts support your theory. There is no evidence to support the theory. Shouldn't you leave this to experts before you give parents more false hopes?

Mary, Trenton, New Jersey.




Dear Mary:

You are right, I am a nobody; just ask my ex-wife. In the Toronto Globe, I explained why I have not yet submitted the paper. As far as giving false hopes, I've thought about that charge. Right now, regardless of what advocacy groups say, autism is rather hopeless. That is, no treatment, including vitamin D, has been shown to materially affect the clinical course of autism. As a psychiatrist, my observation is that people would rather live with a false hope than with no hope.

Furthermore, if autistic children began taking vitamin D, the worse that can happen is that a period of false hope will followed by dashed hopes and then parents will be back to hopelessness. In the meantime, they will have made their child vitamin D sufficient. Vitamin D deficiency is a serious problem in childhood.
Postgrad Med J. 2007 Apr;83(978):230-5.

The Telegraph, Why is Vitamin D So Vital?

As far as the theory having no support from experts, Dr. Richard Mills, research director of the National Autistic Society in England, was quoted in the Telegraph article on the autism/vitamin D theory: "There has been speculation in the past about autism being more common in high-latitude countries that get less sunlight and a tie-up with rickets has been suggested - observations which support the theory."

Finally, you said there is no evidence to support the theory. I assume you meant there is no proof. The first statement is absolutely false, the second absolutely true. As I detailed in my paper, there is a lot of evidence to support the theory. In fact, if anyone can come up with an autism fact, that the theory cannot explain, I'd like to know about it. Even the announcement of a link between television viewing and autism supports the theory. Furthermore, the TV/autism link is actually evidence of a treatment effect. That is, if autistic children who play outside in the sunshine more - watching less TV - have less severe illness, it may be due to the Sun-God, who bestows her precious gift of calcitriol into the brains of children playing outside in her sunlight but not into the brains of children watching TV inside in the darkness.
Natl Bur Econ Res Bull Aging Health. 2007 Winter;(18):2-3.

As far as proof the theory is true, there is, of course, none. In medicine, proof means randomized controlled human trials, the gold standard for proof. However, proof is the last step, not the first. First comes evidence, then comes a theory, then comes researchers disproving those theories. It works that way. Sometimes we never get to the last step, proof. For example, please point me to a single randomized controlled human trial proving cigarette smoking is dangerous? Instead, the convincing evidence of smoking's dangerousness lies in epidemiological studies, not randomized controlled trials. Proof, or disproof, of the autism vitamin D theory will take years, years during which young autistic brains will continue to suffer irreparable damage. Perhaps vitamin D' powerful anti-inflammatory actions will help prevent that damage, perhaps not.

It's something of a Pascal's wager, betting on vitamin D instead of the existence of God, risking your child's brain instead of eternal damnation. "If you believe vitamin D helps autism and turn out to be incorrect, you have lost nothing -- but if you don't believe in vitamin D and turn out to be incorrect, your child will suffer irreparable brain damage."

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

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. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

Michael Pollan Podcast

I just found this great podcast of an April, 2006 National Public Radio (NPR) interview with Omnivore's Dilemma author, Michael Pollan:

Author Michael Pollan: 'The Omnivore's Dilemma'

available at http://www.npr.org/templates/story/story.php?storyId=5342514

The Science Friday segment is a great encapsulation of all the fascinating spins this wonderfully insightful author has on human eating habits and the developing distortions of food choices, much magnified by the food manufacturing industry.

One of my favorite comments from Pollan: "The USDA should be called "The Department of Corn," referring to the ubiquitous dissemination of corn products into livestock and human foods that has increasingly led to the enormous health problems we're all facing in 2007.

Are you addicted to fructose?

Try a little experiment:

Side by side, try a yogurt made with fructose or high fructose corn syrup as one of the first ingredients on the label along with a yogurt made without fructose.

Yoplait and Dannon brands, for instance, fit the bill for fructose. Several brands do not use fructose products. Many of these are the unflavored or unsweetened versions. You may therefore have to add some blueberries, strawberries, or some other fruit for some flavor. ( I doubt that you would add high fructose corn syrup.) Add nuts, seeds, flaxseed, or oat bran to either.

Many people who do this will notice a peculiar effect: The fructose or high fructose corn syrup containing product is, to most, delicious. It also triggers a desire for more. You can't have just one--you've got to have another, or you've got to eat something else.

The non-fructose containing product is more likely to generate satiety, a feeling that you've had enough.

If you experience this effect, the solution is simple: avoid fructose and high fructose corn syrup. I believe that the most worrisome health effect of fructose is this hunger-increasing aspect, difficult to document, perhaps impossible to measure, but a great boon to the food industry who practice an "eat more" philosophy to increase revenues year after year.

Perhaps you will also see weight drop (since you will be more satisfied), see triglycerides drop (since fructose raises triglycerides), and maybe obtain all the downstream benefits of reduced triglycerides (higher HDL, less small LDL, less VLDL, more rapid clearance of post-prandial lipoproteins).

Most people who follow this idea gain better control over appetite, lose weight, and do better in health, including in their Track Your Plaque program.

Chicken Little

Clinical studies can be designed in a number of ways. The ease and cost of these studies differ dramatically, as does the confidence of the findings.

The most confident way to design a clinical study is to tell neither the participants nor the investigator(s) what treatment is being offered, then to administer treatment or placebo. Neither the people doing the research nor the participants know what they are receiving. Of course, there needs to be some way to find out what was given at the end of the study in order to analyze the outcome.

This is called a “double-blind, placebo-controlled” clinical study. While not perfect since it tends to examine a treatment phenomenon in isolation (e.g., the effects of a single drug in a select group of people), it is the best sort of study design that is most likely to yield confident results, both negative and positive. This sort of design is followed, for instance, for most prescription drugs.

There are pitfalls in such studies, of course, and some have made headlines lately. For instance, beyond tending to examine single conditions in a select group of participants, a double-blind, placebo-controlled study can also fail to uncover rare effects. If a study contains 5000 participants, for instance, but a rare complication develops in 1 person out of 20,000, then it’s unlikely such an ill-effect will be observed until larger numbers of people are exposed to the agent.

Another pitfall (though not so much of study design, but of human greed) is that study outcomes that are not favorable can be suppressed by simply failing to publish the results. This has undoubtedly happened numerous times over the years. For this reason, a registry has been created for all human clinical trials as a means to enforce publication of outcomes, both favorable and unfavorable.

Despite its weaknesses, the double-blind, placebo-controlled study design remains the most confident way to show whether or not some treatment does indeed yield some effect. It is less prone to bias from either the participant or the investigator. Human nature being what it is, we tend to influence results just to suit our particular agenda or interests. An investigator who knows what you are given, drug or placebo, but owns lots of stock in the company, or is hoping for special favors from the pharmaceutical company sponsor, for instance, is likely to perceive events in a light favorable to the outcome of the study.

Now, most studies are not double-blind, placebo-controlled studies. These are notoriously difficult studies to engineer; raise lots of ethical questions (can you not treat a person with an aggressive cancer, for instance, and administer a placebo?); often require substantial numbers of participants (thousands), many of whom may insist on payment for devoting their time, bodies, and perhaps even encountering some risk; and are tremendously expensive, costing many tens of millions of dollars.

For this reason, many other study designs are often followed. They are cheaper, quicker, may not even require the active knowledge or participation of the group being studied. That’s not to say that the participants are being tricked. It may simply be something like trying to determine if there are more heart attacks in people who live in cities compared to rural areas by comparing death rates from heart attack from public records and population demographic data. Or, a nutritional study could be performed by asking people how many eggs they eat each week and then contacting them every month for 5 years to see if they’ve had a heart attack or other heart event. No treatment is introduced, no danger is added to a person’s established habits. Many epidemiologic studies are performed this way.

The problem is that these other sorts of study designs, because they generate less confident results, are not generally regarded as proof of anything. They can only suggest the possibility of an association, an hypothesis. For real proof to occur, a double-blind, placebo-controlled may need to follow. Alternatively, if an association suggested by a study of lesser design might, by reasons of a very powerful effect, be sufficient. But this is rare. Thalidomide and catastrophic birth defects are an example of an association between a drug and fetal limb malformation that was so clear-cut that no further investigation was required to establish a causative association. Of course, no one in their right mind would even suggest a blinded study.

Where am I going with this tedious rambling? Lately, the media has been making a big to-do about several studies, none of which are double-blind, placebo-controlled, but were cross-sectional sorts of observations, the sorts of studies which can only suggest an effect. This happened with Dr. Steve Nissen’s study of Avandia (rosiglitazone) for pre-diabetes and risk for heart attack and the recent study suggesting that cancer incidence is increased when LDL cholesterol is low. Both were observations that suggested such associations.

Now, those of you following the Heart Scan Blog or the www.cureality.com website know that we do not defend drug companies nor their drugs. In fact, we’ve openly and repeatedly criticized the drug industry for many of its practices. Drugs are, in my opinion, miserably overused and abused.

But, as always, I am in the pursuit of truth. Neither of these studies, in my view, justified the sort of media attention they received. They are hypothesis-generating efforts—that’s it. You might argue that the questions raised are so crucial that any incremental risk of a drug is simply not worth it.

Despite the over-reaction to these studies, good will come of the fuss. I do believe that heightened scrutiny of the drug industry will result. Many people will seek to avoid prescription drugs and opt for healthy changes in lifestyle, thus reducing exposure to costs and side-effects.

But beware of the media, acting as our Chicken Little, reporting on studies that prove nothing but only raise questions.

200 point drop in heart scan score

Some of the math-savvy will have noticed that we often report drops in CT heart scan scores on a percentage basis. Unfortunately, it this were a competition (which, of course, it is not), this would be unfair.

A score of 50, for instance, that drops "only" 25 points would represent a 50% drop in score.

But someone with a score of 1050 who drops his or her score the same quantity, or 25, will have dropped their score less than 5%.

In other words, the magnitude of your starting score determines how large a percentage drop you achieve, even when the absolute, or real, quantity of plaque reversal is the same as someone who begins with a lower score.

I qualify this discussion in this vein because of Grady's story. Grady, a soon-to-retire attorney, started with a heart scan score of 1151. On the Track Your Plaque program, he saw his score drop nearly 200 points--200 points!

But, if we gauged Grady's success just on a percentage basis, he dropped his score only a measly 17% or so. (Imagine the headlines if this program were sponsored by a drug manufacturer. The Track Your Plaque program proudly has nothing to do with the drug industry.)

Of course, the Track Your Plaque program is not a competition. It is an effort to help everyone possible, the more the better. Even if Grady failed to set a new Track Your Plaque record gauged on a percentage basis, he will have achieved an extraordinary advantage in health: the virtual elimination of the dangers of heart disease.

With this drop in score, Grady's risk for heart attack plummets from a spine-chilling 25% per year to nearly zero. (I know of NO other program that can claim such a track record.)

Grady's full story will be reported in the August, 2007 Track Your Plaque newsletter. To subscribe or to just view when it is posted, go to www.cureality.com website, click on the upper right hand corner What Does My Heart Scan Show? graphic, which then takes you to the page to view the newsletter. Or, Track Your Plaque Members can just go to the Library and click on newsletter archives.

How tough is the Track Your Plaque 60-60-60 target?

One of the basic requirements that stack the odds in your favor of stopping or dropping your CT heart scan score is to achieve basic lipid targets of 60-60-60.

In other words, we generally see best results when LDL is reduced to 60 mg/dl, HDL raised to 60 mg/dl, triglycerides reduced to 60 mg/dl. Now, these are not absolute requirements. Someone can have a spectacular drop in heart scan score even with an HDL of 56, LDL of 71. But the "Rule of 60" provides a useful target that is easy to remember, packs real power, and is clearly beyond that achieved with conventional approaches.

People often ask, "Just how tough is it to get to these targets?"

It's really not that tough. Interestingly, whenever I tell my cardiologist or primary care colleagues that I advocate these 60-60-60 targets, they declare that it's tough, perhaps impossible, except for the most highly motivated.

I agree that it requires motivation. A cigarette-smoking, TV-addicted, 70-lb overweight, chip- and pretzel-eating couch potato is not going to achieve them.

On the other hand, you don't have to be a marathon running vegetarian to do it, either.

Most people, in fact, engaged in the Track Your Plaque program achieve the 60-60-60 targets---or exceed them. It's not uncommon, for instance, for HDL to skyrocket to 80 or 90 mg/dl with many of our strategies. (Of course, if your starting HDL is 20 or 25 mg/dl, 80 or 90 is not possible with current technology.)

But it certainly does require more than the "Take Lipitor and stick to your low-fat diet" approach that is the mantra repeated in the vast majority of medical offices across the U.S. For instance, reducing LDL to 60 mg/dl when starting at 170 mg/dl will require addition of oat bran and other soluble or viscous fibers; raw almonds and walnuts; perhaps the use of Benecol butter substitute; reduction or elimination of wheat products if small LDL comprises a substantial proportion of LDL particles. Reducing triglycerides requires the generous use of omega-3 fatty acids from fish oil. Attention to vitamin D must be a part of the effort.

So, yes, it is not as simple as the conventional approach. But the results are far superior in reducing or eliminating heart attack and in dropping your heart scan score.

But it can be done. We do it every day.

Vitamin D2 belongs in the garbage

It happened yet again.

Mel came to the office. CT heart scan score: 799--quite high, enough to pose a real threat very soon. Thus, no time to lose in instituting an effective prevention program.

We do the usual--identify the six causes of coronary plaque; begin fish oil, show him how to correct his plaque causes. You've heard it before.

Vitamin D blood level in March: 17 ng/ml--severe deficiency.

Vitamin D replacement needs to be a part of his coronary plaque control program. So I suggested 6000 units per day of an oil-based preparation of vitamin D3 (cholecalciferol). Conveniently, there is a Vitamin Shoppe outlet across the street from my office. I just point and tell people to go across the street.

Mel did just that. However, he also informed his primary care physician about his vitamin D deficiency. His primary physician promptly told him he needed to take a prescription form of vitamin D and not to bother with just a supplement.

So Mel stopped his vitamin D capsules and started taking vitamin D prescription "medication." Mel figured, naturally, that if it requires a prescription, it must be better. Unfortunately, Mel and his doctor failed to pass the change in strategy onto us.

So, four months later, Mel got repeat vitamin D blood level: 19 ng/ml.

I've seen this too many times. The prescription form of vitamin D is nonsense. There's hardly any effect on blood levels of vitamin D3 at all. The body's conversion of this non-human form of D is extremely inefficient and therefore virtually useless. While it raises the blood level of vitamin D2 (ergocalciferol) and thereby total D (D3 + D2), there is negligible effect on the real human and active form, D3.

How and why this preparation got through the FDA process to obtain approval as a drug is beyond me, though I am not a defender of FDA practices and politics.

This notion that "if it's a prescription, it must be better" is a fiction perpetuated by the drug industry. The same principle gets tossed around with fish oil, hormones like estrogens and testosterone, and others. Often, the principal difference between prescription and non-prescription is patent protection. Patent protection provides profit protection. Selling a product without patent protection can be risky business. It's certainly less profitable.

As always, getting at the truth is sometimes the most difficult job of all. Prescription vitamin D belongs in the garbage. Vitamin D capsules (gelcaps) do the job and do it well, over and over, with reliable, consistent and substantial rises in blood levels of 25-OH-vitamin D3. I take 6000 units per day (3 2000 unit capsules) that cost me $5.99 for a bottle of 120 capsules, or about $4.50 a month.

And nobody--nobody--pays me to say this. I say it because I believe it's true.

Angioplasty vs. Track Your Plaque

What does angioplasty have over the Track Your Plaque program?

Well, first of all, the Track Your Plaque program has a lot to boast about. What other approach can claim to have reduced heart disease 30, 40, 51, and now 63%? That's as close to a cure that's ever--EVER--been achieved. Statin drug manufacturers can talk about an occasional 1, 2, or 5% reversal. We're talking 10 times more.

The Track Your Plaque program also uses as little prescription medication as necessary. Fish oil, vitamin D, coenzyme Q10, niacin--some of the frequent tools used for plaque reversal in our program. Yes, we do use prescription medications, but only when there is truly a benefit and nutritional strategies have failed to achieve the goals we're seeking. We do not endorse shotgun prescription approaches conceived of by some marketing department at a pharmaceutical company.

So what possible advantage can coronary angioplasty have? Why don't more people embrace a program like Track Your Plaque that has already proven itself enormously effective?

Because angioplasty is easy. There's little worrying ahead of time. Just wait for the symptoms or other problem to appear, go to the hospital and get your procedure. You can live the free and easy life beforehand--no exercise, no diet efforts, no nutritional supplements. Just be sure to go to the hospital when suspicious symptoms strike. (Of course, you gamble that you survive the appearance of symptoms, a process 30-50% of people fail to survive.)

That means you can eat all you want, drink all you want, save the money you otherwise might have thrown away on supplements, pocket the monthly costs of an exercise club membership, etc. Go to the hospital when you experience the sensation of an anvil on your chest or of suffocation, let the emergency room do their thing, meet your cardiologist, go to the catheterization laboratory, get two or three stents, go home the next day!

Why bother with a prevention program, especially one that requires involvement, learning, and effort like Track Your Plaque?

Because it's your way to stack the odds enormously in your favor of 1) surviving the appearance of symptoms, 2) avoiding the prospect of heart procedures, which are not as clean and easy as they often seem, 3) have a longer lasting durability than a stent which could buy you a couple of years before your next procedure or heart catastrophe, and 4) it's the right thing to do for the sake of the huge societal cost of heart disease.

Many of you have the equivalent of a cure for heart disease at your fingertips. Unless you have a soft spot in your heart for hospitals, cardiologists, or the pharmaceutical or medical device industry, there isn't a choice.

Plaque is like money

In case anyone missed this in the June, 2007 Track Your Plaque Newsletter, I'm again posting how we calculate the annual rate of score increase, should it occur.

For instance, say your score in January, 2005, is 100. In November, 2006, you undergo another scan and the score is 140. Obviously, your score has increased an undesirable 40%. But what is the annual rate of score increase, the amount of increase per year?

In this example, the annual rate of score increase is 19%--not anywhere near as bad as the 40% that can scare the heck out of you.

Obviously, the best rate of heart scan score increase is a negative number, i.e., a drop in score from, say 100, to 60. You might even eliminate the need for this calculation altogether if you drop your score.

Nonetheless, whenever there is a score increase over an uneven period of time, a fraction of year(s), this is the method we use to annualize the calculation. The equation we use is a modified form of the annual compound interest equation using continuous compounding, since that’s how coronary atherosclerotic plaque grows--just like money. The difference is, of course, is that while you might want more money, you certainly don't want more plaque.

You will need a calculator for this calculation, one with an exponential “y to the power x” function. For ease, calculate "1/t first, then use it as the “x” exponent on your yx function and "(score 2 / score 1)" as the "y".


Annual rate of plaque growth (APG) = ( score 2 / score 1 ) 1/t - 1

Multiply the result by 100 to yield a percent.


“Score 1” is your 1st heart scan score, “score 2” is your 2nd (or any subsequent heart scan score); “t” is the amount of time between the two scans expressed in years in decimal form. Time between scans should be expressed in years or fractions of years. To obtain the time interval in fractions of years, simply divide the number of months between scans by 12 (e.g., 18 months / 12 = 1.5 years ; 22 months / 12 = 1.83 years).

It’s not as tricky as it looks. For example, if your first heart scan score is 300 and your next scan 16 months later (or 16/12 = 1.33 years) is 372, then:

Annual rate of plaque growth (APG) = ( 372 / 300 ) 1/1.33 - 1 = 0.175

Multiply 0.175 x 100 = 17.5% annual rate of plaque growth


Some scan centers will do the calculation for you as part of a repeat scan. However, the equation can be used if you're left on your own, or if you go to a different scan center. If this is too much effort, perhaps it's just another reason to add to the list of reasons to drop your heart scan score!

Triglycerides: What is normal?

In The Track Your Plaque program, we advocate decreasing triglycerides to 60 mg/dl or less.

That's the level of triglycerides that minimize the presence of triglyceride-containing undesirable lipoproteins causing plaque, such as small LDL, VLDL, and the after-eating persistence of IDL (intermediate-density lipoprotein, a bad player). (The enzyme, cholesteryl-ester transfer protein, or CETP, is responsible for exchanging one triglyceride molecule for one cholesterol molecule between HDL and other lipoprotein particles. Thus, an excess of triglyceride availability permits CETP to operate unrestrained, creating more undesirable lipoproteins. This was the basis for Pfizer's now defunct CETP inhibitor, torcetrapib.)

Of course, this triglyceride target is far below that of the conventional guidelines. The Adult Treatment Panel-III of the National Cholesterol Education Panel suggests a triglyceride level of 150 mg/dl is okay.

In my view, a level of 150 mg/dl is highly abnormal, permitting the persistence of multiple lipoprotein particles and virtually guarantees plaque growth. In short, triglycerides of 150 are awful.

Curious thing: Successful participants in our program, i.e., people who achieve desirable weight, reduce processed carbohydrate junk foods and saturated fat sources, and aim for the 60-60-60 targets for conventional lipids, commonly end up with triglyceride levels of 25-50 mg/dl.

We have seen many people drop their heart scan scores just by achieving a triglyceride level of 60 mg/dl or less. So achieving a lower level below 60 is not necessarily a requirement for coronary plaque regression.

But it makes me wonder if a triglycere level of 30s or 40s is the level for perfect health. These are levels ordinarily regarded as impossibly low. When colleagues see the numbers we readily and routinely achieve, they declare that the numbers are spurious, temporary, or just flukes. "No way you can do that all the time!"

This level also seems to, in virtually all cases, eliminate the triglyceride-containing undesirable lipoproteins small LDL, IDL, etc., and allow full conversion of HDL into the healthy, large fraction.

Should we move the Track Your Plaque triglyceride target to below 45 mg/dl or even lower? I don't think so, but it makes me wonder.
All posts by william-davis

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

60-year old man dies of high cholesterol

Never saw a headline like this? Neither have I. That's because it doesn't happen.

Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.

Back to basics: Coronary calcium

After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.

Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.

If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.

Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)

But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.

Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.

There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.

So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.

But it's the best we've got.

If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.

Myocardial infraction

I've seen a few heart attacks this past year . . . but none in the people who follow this program.

I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day.

I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind.

A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive."

There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates.

In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.

Diet is superior to drugs

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.


(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Low-carb is heart healthy

Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.

First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension.

Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk.

In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:

Reduced fasting triglycerides and VLDL
Reduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnants
Increased HDL and shift towards large HDL particles (presumably more protective)
Reduced small LDL particles
Reduced glycation and oxidation of small LDL particles
Reduced hemoglobin A1c
Reduced c-reactive protein and other inflammatory markers
Reduced blood pressure

By slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis.

Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.

Mocha Walnut Brownies

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . .  . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.


Ingredients:
8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)


Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.