Wheat-free and still fat

Readers of The Heart Scan Blog know that I preach a diet that contains foods with low glycemic index to control weight, raise HDL, and reduce triglycerides, blood sugar, and small LDL.

A crucial aspect of a low glycemic index approach is to sharply reduce, preferably eliminate, wheat products.

I pick on wheat specifically because it has come to dominate the American diet. Look at the shelves in the supermarket: aisle after aisle of processed wheat products. The bread shelves alone in some of the grocery stores in my neighborhood are 40 feet long, six shelves high. There's also breakfast cereals, granola products, cookies, cakes, baking products, pretzels, crackers, pasta, and on and on.

Wheat products like these are tasty and they're addicting--literally. Test animals given processed wheat will eat more and gain more weight. Wheat fails to trigger satiety. So laboratory mice--and you and I--eat and eat, because eating wheat stimulates appetite, creates a hunger for more wheat, and a vicious cycle ensues. Eliminating wheat, on the other hand, results in dramatic drop in appetite, substantial weight loss, followed by correction of the metabolic disruptions it created.


A quick Google search for "gluten-free" turns up a startling array of wheat-free, gluten-free, yet high glycemic index products. The breakfast cereal pictured, for instance, can do as much damage as most wheat containing products--though it won't cause gluten enteropathy (also known as "celiac disease").




The product shown contains:

Brown rice flakes, rice bran, evaporated cane juice, brown rice syrup, raisins, cinnamon, gum arabic, vanilla, molasses, ground flaxseed, rosemary extract.

A 1/2-cup serving contains:
Total Carbohydrate 31g
Dietary Fiber 5g
Sugars 8g


And I'll bet that most people eat a lot more than a half-cup serving.

But you and I are not laboratory mice. If deprived of wheat, many people will then seek out processed rice products (rice cakes, Rice Krispies), processed cornstarch or cornmeal products (tacos, cornbread, many processed foods using these products for texture or thickness), or other products labeled "gluten-free."

Going wheat-free for our purposes is not about avoiding the gluten in wheat. It is about seizing control of appetite, eliminating a food that disrupts insulin responses, reduces HDL, raises triglycerides, and creates small LDL particles. But this applies to processed corn, rice, and other high glycemic index foods, as well.

So, occasionally, someone will declare, "I've eliminated wheat! Now I only eat rice, corn, and I've discovered all the gluten-free alternatives!"

Unfortunately, they've traded one evil for another. So it's not just about wheat. It's really about reducing or minimizing foods that mess up metabolic responses and lead to coronary plaque growth. Wheat is the biggest culprit and so I focus on it. However, you could easily transfer far less popular rice and corn products into center stage and allow them to wreak all the health damage of wheat.

Going wheat-free for our atherosclerotic plaque-control purposes is not the same as going gluten-free. So be careful of the distinction.


Wheat-free gummi bears:


Contents:
Organic dehydrated cane juice, organic corn malt syrup, organic juice concentrates (may contain organic apple, organic apricot, organic aronia, organic carrot, organic cranberry, organic elderberry, organic lemon or organic red beet), organic spinach powder, organic apple pectin, citric acid, natural fruit flavors.

Virtually pure sugar--yet wheat-free.



Wheat-free rice bread


Ingredients:
White rice flour, water, honey, soy oil, natural gum, salt, yeast, natural gum














Copyright 2008 William Davis, MD

Heart disease is reversible

In a previous post, Take this survey: I double-dare you, I posed a challenge:

Ask your doctor: Is heart disease reversible? Their answer:

1) No. Heart disease is definitely not reversible.

2) Yes, in rare instances, like lightning striking twice.

3) Yes, of course it is! Let's talk about how to do it!

I predicted that few readers of this blog would respond. I also predicted that the few who did would respond with the first answer, Heart disease is definitely not reversible. After all, in nearly all medical practices, the only parameters routinely followed to track risk for heart disease are LDL cholesterol and blood pressure. A measure of the disease itself (i.e., coronary atherosclerotic plaque) is not followed. So how can your doctor actually tell whether heart disease is reversed or not? When I engage in this conversation with colleagues, it goes no farther than rolled eyes or a snort. In my experience, talking about reversal of heart disease is a wasted effort.

To my great surprise, this simple survey received a total of 177 responses. Even more surprising, 122 (69%) of respondents chose number 3, claiming that their doctor said that heart disease is reversible.

Overall results:

1--31 responses (17.5%)

2--24 responses (13.5%)

3--122 responses (69%)


Now wait a minute: Where is the disconnect? Why are doctors saying that heart disease is reversible, yet not following this concept in practice? Contrary to the survey results, I have yet to meet a patient who said their doctor was trying to reverse their heart disease. Of course, this may be a skewed population, but I find it hard to believe that the prevailing view is that heart disease is reversible.

Anyway, this simple survey cannot settle the why or how, nor can it suggest just how prevalent this opinion is.

I am encouraged by these results. If true, it means that the message that heart disease is a reversible process is spreading. It may be make-believe heart disease reversal as preached by Dr. Dean Ornish or claimed by statin drug manufacturers. It may be the hocus-pocus of practices like chelation, or scams like nattokinase. But perhaps the seed of this notion has been planted in the minds of the medical community.

I'd be interested in hearing from the respondents who reported that their doctor said heart disease is reversible. How exactly are they going about achieving reversal?

Looking for health in all the wrong places

The American public now has unprecedented freedom to explore new directions in health.

Never before have we had the enormous resources now available to add to our health experience: nutritional supplements, endless books on health and diet, the internet, online discussion groups, insurance products to permit spending on self-directed health services like medical savings accounts and flex-spending. The Track Your Plaque program is just one facet of this emerging and exciting area of self-empowerment in health. Compare what you can achieve with such a program with the situation of just 25 years ago, when the most you might get to reduce your risk for heart disease was to take the (largely ineffective) drug cholestyramine, probucol, and a low-cholesterol, low-fat diet.

Unfortunately, it also means that people have unrestrained potential to be tripped up, to be misled down some dead end of health that fails to accomplish desired goals, maybe even dangerous. The more freedom we have, the greater the choices, the more room we have to screw up.

Among the unproductive strategies I've witnessed recently:

--Nattokinase--The staying power of this scam continues to shock me. There is no rational basis for its use. A woman today declared that she would like to stop the warfarin that she was taking to prevent stroke from atrial fibrillation by taking nattokinase. This would be a mistake that could cost her a major and disabling, even fatal, stroke. Though warfarin is far from perfect, it at least achieves its goal of reducing stroke risk. Nattokinase does not. Nattokinase does nothing but make money for the people who sell it.

--Poly-nutritional supplements. You've heard of polypharmacy, the phenomenon of taking numerous medications with overlapping effects and side-effects, usually because of multiple doctors, each prescribing drugs without knowledge or interest in what colleagues are prescribing. I'm seeing the same phenomenon with supplements: 20,30, or more supplements per day, all in the hopes of heightening health. A focused few supplements is, in my view, superior to a shotgun approach of trying to improve health by taking hawthorne, silymarin, chrysin, calcium, Chinese herbs, and 25 other supplements.

--Chelation--Based on the notion that heavy metal toxicity causes heart disease; removal of heavy metals cures it. I've read some of the books on chelation, in addition to the slim scientific data, to decide whether there was anything to it. In my view, it is a complete and utter scam. It does make money for its practitioners, however. That's not to say that heavy-metal chelation doesn't have a role in health--it does. But it serves no purpose in coronary disease prevention and control.

--Colonic purges--Achieved by a number of routes, some oral, others via enema. Promotions for purging are often accompanied by a pile of scum that apparently lined somebody's intestinal tract. Purges purportedly, well, purge it from the intestine. This is also plain nonsense. There is no such toxic scum lining anybody's intestinal tract. However, if calorie restriction or a fast results inadvertently from the effort, perhaps some good comes from it.

--Statin drug alternatives--The unprecedented $27 billion dollar a year success of the statin drug industry, accompanied by the enormous marketing push by their manufacturers, has spawned an entire industry of statin alternatives. They range from red yeast rice, to guggulipid, to various concoctions of sterol esters, Chinese herbs, chitosan, and a variety of others. Some actually do reduce cholesterol a few points. Preparations like red yeast rice even pose a side-effect profile not too different from the prescription statin agents. Unfortunately, even among those agents that work, the effects tend to be small to trivial. While I am no lover of statin drugs nor the statin drug industry, I find these preparations to be anemic imitators. You'd be better off with raw nuts and ground flaxseed than wasting your money on these cheap imitations.

--Worries about liver toxicity--A day doesn't go by that I don't have at least several questions about suffering toxic liver effects from niacin, vitamin D, statin drugs, etc. I have treated thousands of patients for heart disease in its various stages and forms and have used many different strategies. How many times have I seen serious liver toxicity? A handful of times and usually from either mis-use of the agent or drug, or in a person with several other coexisting diseases. (Other serious health conditions, like kidney failure, raise the toxicity of drugs and supplements.) Liver toxicity in the vast majority of otherwise healthy people is close to being a non-concern.


Readers of The Heart Scan Blog and of the Track Your Plaque website know that I celebrate expansion of knowledge and information access to the public. However, I am concerned that the flip side of this growing self-empowerment is expanding potential for mistakes. It reminds me of an attorney friend, who, when diagnosed with prostate cancer, explored all manner of alternative treatments, from laetrile to heavy metal chelation to high-dose lycopene tablets. At the initial stage of diagnosis, his cancer was readily treatable. He now has widely metastatic cancer.

Maintain an open mind, but think before you commit to some crazed claim of cure, some "secret" to health, somebody's brazen but concealed attempt at steering profits in their direction.

With freedom comes responsibility. Otherwise, you might be looking for love . . .oops, I mean health . . . in all the wrong places.

Track Your Plaque APB

I'm posting this intriguing comment from the Track Your Plaque Member Forum because I would like to speak to the Member who posted it.

The Member said:

I tested at 965 last year, and while I have followed the TYP diet and nutraceutical recommendations, I was totally unprepared for my first repeat scan (at the same lab/machine) on January 29, 2008. My result was 4.0, and at first I assumed the rating scale had been changed.

I then noted that 3 of the big four arteries received scores of 0, which means the same in any scale, and that four nodules had disappeared from the scan field.



Wow!!

If this is true, it would represent the biggest success in the Track Your Plaque program--ever! It would be an incredible story to tell, to convince the public and medical community that it is indeed possible, and a cause for popping a bottle of champagne! It would also represent what I would regard as essentially a cure for coronary atherosclerosis, a virtual elimination.

While we have plenty of success in stopping the progression or reducing heart scan scores, we do not have 100% success. I wish we did. The Track Your Plaque program is, to some degree, a work in progress. We learn from experiences, continually adjust to obtain the results we desire. Even as it stands today, the Track Your Plaque program is superior to any program of heart disease prevention known--by a long stretch. But it's not infallible, it's not foolproof.

That's all the more reason I would like to communicate with the Track Your Plaque Member who posted this comment. I would also like permission to view the heart scans themselves. (I can't obtain them nor view them without the individual's permission.) While we often have difficulty judging reversal just by looking at heart scans, presumed reversal to this profound degree should be obvious, even to the naked eye.

I would like to know--in detail--precisely what steps were taken and whether there was anything unique about this person's medical history or in the program they followed. This is all in an effort to learn and help others do the same.

If you are the Member who posted this comment, I would like to hear more. Please post your further thoughts on the Track Your Plaque Member Forum, or privately through our Contact page . Or e-mail us at contact@cureality.com.

Vitamin D toxicity

It is the craziest thing.

The notion of vitamin D being easily and readily toxic has grabbed hold of many people, including my colleagues who were taught that vitamin D was toxic in medical school based on the skimpiest (and often misinterpreted) observations in a handful of unusual cases.

In my practice and in the Track Your Plaque program, we routinely use doses of 2000-10,000 units per day, occasionally more. We are guided by blood levels of 25(OH) vitamin D3. I have personally never witnessed vitamin D toxicity.

Here's an interesting graph from Dr. Reinhold Vieth. Those of you familiar with the vitamin D argument know that Dr. Vieth is among the few genuine gurus in the vitamin D world.



















From Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842-856. (Full text is available without charge.)

In the graph, the X's represent toxicity; circles fall within the non-toxic range. (Toxicity is generally defined as a level sufficient to raise blood calcium levels, "hypercalcemia.") Note that the 25(OH) vitamin D3 levels are given in nmol/L; to convert to ng/ml units that are customary in the U.S., divide the nmol/L value by a factor of 2.5.

You will notice that toxicity is virtually unheard of until the dose exceeds 10,000 units per day. Beyond 10,000 units per day, the curve heads upward sharply and toxicity does become a possibility, though not an absolute (since there are circles above 10,000 units).

You may also notice that the curve is relatively flat from vitamin D doses between 200 units and 10,000 units (log scale on x axis; arithmetic scale on y), the range of most common doses for vitamin D supplementation.

Another perspective on vitamin D blood levels is to examine the blood levels of people who are young and obtain plentiful sun exposure. Lifeguards, for instance, have blood levels of 84 ng/ml (210 nmol/L) without ill-effect. (Sun exposure cannot generate vitamin D toxicity, because of a feedback safety mechanism in skin.) While this may not represent an ideal level since they represent an extreme, it does provide reassurance that such levels are non-toxic. I also point out these levels occur in the youthful since most people lose 75% or more of vitamin D activating capacity in the skin by their 70s. Most of us over 40 are kidding ourselves if we think that a suntan provides sufficient vitamin D.

Keep in mind that it is not necessarily the dose of vitamin D that is toxic, but the blood level it generates. I take 10,000 units of vitamin D as a gelcap per day to maintain my blood level between 50-60 ng/ml (125-150 nmol/L). This strategy helps me keep my HDL in the 70-80 mg/dl range, my blood sugar around 90 mg/dl, my blood pressure <120/80, and I no longer experience colds nor winter "blues."


Copyright 2008 William Davis, MD

Turning plaque into profit

For reasons unknown to me, I received a solicitation to invest in a company called Prescient Medical, with a slogan that caught my eye:


Detect and treat heart attacks before they occur.


The glossy brochure details their technology development strategy:

Predict(TM) Optical Catheter System--A catheter introduced into the coronary artery during a catheterization procedure to determine whether a specific plaque or vessel area is "vulnerable," i.e., prone to rupture in future.

Protect(TM) Luminal Shield--A stent-like metal device deployed into the coronary artery at the region of vulnerable plaque to prevent future plaque rupture.

The company anticipates FDA approval for their systems by 2009 and sales to begin by 2010. They predict sales of $7 billion.

Let's stop and think about this for a moment. It seems to me that, rather than pursuing the market of another stent for a "severe blockage," this company is going after the untapped procedural market of vulnerable plaque. In other words, their technology (an optical sensor technology that emits and analyzes light wavelengths to map specific plaque characteristics) identifies plaque that may rupture in months or years, followed by implantation of stent(s) that presumably prevent plaque rupture.

Thus, conceivably, many 20%, 30%, 40% etc. "blockages", atherosclerotic plaques that do not block flow and thereby pose no need for a conventional stent, will end up with this new type of stent. One patient could therefore receive multiple "Luminal Shields" in a single procedure.

When would these devices be employed? One pathway I could conceive of that my colleagues will be sure to exploit is 1) identify plaque by CT angiography, then 2) bring patient to the catheterization laboratory and perform this procedure for whatever hot, vulnerable plaques are identified. In other words, symptoms are no longer necessary. Reduced blood flow is no longer necessary. An abnormal stress test is no longer necessary. All that is required is that you have plaque. If the plaque is then determined to be vulnerable, then it is stented.

What bothers me about all this is the emerging effort to exploit this untapped market--a big one--of early heart disease as identified by coronary atherosclerotic plaque. As heart scans have demonstrated, there is an enormous amount of hidden heart disease in this world. This company has discovered a way to turn plaque into a profit opportunity, much as the statin drug industry found a way to "turn cholesterol into money."

The conventional stent market has plateaued and now has been, to some degree, battered by the drug-coated stent argument. Prescient has found a new and significant market for procedures and stents.

Is this really necessary? Why does plaque have to become a procedural disease? Doesn't it make more sense that, if vulnerable plaque is identified, that clinical trials are then designed to develop treatment strategies that modify vulnerable characteristics? Shockingly, this has not been done to any significant extent. Instead, the easiest path to a profit opportunity is to implant a "Luminal Shield."

You and I are able to inactivate, disempower, and essentially shut down plaque, while others are working furiously to convert it into a procedural profit opportunity. I personally find this so distasteful that I would sooner endorse a high-dose statin strategy than this approach.

You can view a video of my colleague, Dr. Martin Leon, on the Prescient Medical website, (or click here to go directly to the video), talking about how this technology will "change the treatment paradigm of the interventionalist from reactive to proactive." Scary stuff. Dr. Leon has made millions of dollars (probably more like tens of millions of dollars) from his support of technology companies for the interventional coronary device market.

My hope is that word of the sorts of techniques we use in the Track Your Plaque program disseminate before this sort of luminal coating idiocy gets off the ground.

(In actuality, a different version of this approach has been available for years using intravascular ultrasound (IVUS), another procedure that involves threading a catheter down each coronary artery during a catheterization procedure. IVUS can also cross-sectionally map a plaque's anatomy and identify "vulnerable" features, like a thin cap overlying a collection of semi-liquid fat ("lipid pool"). There has been some discussion of using this approach to identify vulnerable plaque followed by stent implantation, but it has never gotten off the ground and has certainly not found validation in any clinical study. By the way, any stent prevents plaque rupture, since by their very nature, the plaque contents are compressed, modified, and excluded to the exterior of the stent. Plaque rupture within a stent is very rare in its few millimeters of length. It may therefore not require some new technology to prevent plaque rupture.)

Statin mono-failure

Evan's first heart scan score in November, 2006 yielded a high score for a 56-year old male: 542.

So he put up little fuss when his doctor prescribed simvastatin at a high dose.

Evan's LDL cholesterol before simvastatin: 158 mg/dl

Evan's LDL cholesterol on simvastatin: 72 mg/dl.

By conventional standards, Evan has had an excellent response. The rest of his lipid (cholesterol) panel was unrevealing: HDL 62 mg/dl, triglycerides 78 mg/dl. Evan doesn't smoke, has a normal blood pressure, and he is not diabetic. That should do it, right?

So his doctor thought. So Evan asked if another heart scan was in order. In December, 2007, after one year of simvastatin, his second heart scan score: 705--a 30% increase over one year.

Recall that, with no effort at prevention whatsoever, the natural progression of heart scan scores is a 30% per year increase. Did simvastatin do nothing?

This is quite typical of people who do nothing more than take a statin drug. While some people do slow plaque growth (we say "decelerate") modestly on a statin drug, Evan's experience is not unusual: plaque continues to grow despite high-dose statin drug and an apparently favorable cholesterol panel.

In fact, I can count the number of people who reduced their heart scan scores taking a statin drug alone on one finger.

Statins do not represent a cure for heart disease. They cannot be used as sole therapy to reduce risk for heart attack. In fact, given sufficient time, the majority of people who do nothing more than follow this standard line of treatment (along with the equally lame low-fat diet, etc.) will have done nothing more than postpone their heart attack. Elimination of risk? Nope.

This is among the reasons we developed the Track Your Plaque approach. While not foolproof, I know of no better approach to seize control over plaque growth.

Additional conversations on clinical studies which, as with Evan's experience, demonstrated how statin drugs fail to slow plaque growth can be found in previous Heart Scan Blog posts:

Don't be satisfied with "deceleration"

Study review: Yet another Lipitor study



Copyright 2008 William Davis, MD

Triglyceride traps

Triglycerides are a potent trigger for coronary plaque growth.

Triglycerides in and of themselves probably do not cause plaque growth. Instead, triglycerides contribute to the formation of abnormal lipoproteins in the blood that, in turn, trigger coronary plaque, like VLDL, intermediate-density lipoprotein (IDL), and small LDL. Excess triglycerides also modify HDL structure and cause you to lose HDL in the urine.

I see plenty of people who begin with triglycerides of 200 mg/dl, 300, 700, even over 1000 mg/dl. It doesn't take long before you learn what works, what doesn't to reduce triglycerides. This is especially true in the Track Your Plaque approach, in which our target for triglycerides is 60 mg/dl or less.

Here's a list of things to consider if you are trying to gain control of your triglycerides:

--Fish oil--A mainstay of treatment. The omega-3 fatty acids from fish oil are the number one most potent treatment for high triglycerides.

--Reduction of high-glycemic index foods--Most notably wheat. Everybody knows that we shouldn't eat Snickers bars or bags of licorice. But many people eat plenty of wheat-containing breads, pastas, pretzels, crackers, breakfast cereals, etc., all in the name of increasing whole grains and fiber. In reality, they are causing triglycerides to skyrocket, dropping HDL, forming small LDL, increaaing blood sugar and blood pressure, and increasing obesity.

--Eliminating fructose and high-fructose corn syrup--This ubiquitous sweetener is now consumed in enormous quantities by the average American, nearly 80 lbs per year per person. You'll find it in soft drinks, ketchup, beer, breads, breakfast cereals, and many other processed foods. You'll find none in green peppers, cucumbers, and raw nuts. Fructose causes large rises in triglycerides, as well as diabetic patterns. Don't let "fat-free" claims fool you. Take a look at the ingredients in Kraft Fat-Free Caesar Italian salad dressing, for instance:

Kraft Fat-Free Caesar Italian

Ingredients:
Water, Vinegar, High Fructose Corn Syrup, Corn Syrup, Salt, Parmesan Cheese, Part-Skim Milk, Cheese Culture, Salt, Enzymes, Contains less than 2% of Garlic, Whey, Onion Juice, Autolyzed Yeast Extract, Phosphoric Acid, Worcestershire Sauce, Vinegar, Molasses, Corn Syrup, Water, Salt, Caramel Color, Dried Garlic, Sugar ,Spices, Tamarind, Natural Flavors, Hydrolyzed Soy Protein, Xanthan Gum, Potassium Sorbate and Calcium Disodium EDTA as Preservatives, Dried Garlic, Buttermilk, Spice, Dried Parsley, Caramel Color, Sodium Phosphate, Oleoresin Paprika.



--Alcohol--While a couple of drinks a day raises HDL, exerts anti-inflammatory effects, and reduces blood pressure, more than this begins to raise triglycerides. Although I've come across no formal studies on this question, my gut sense is that beer, in particular, raises triglycerides more than wine or other alcoholic beverages. Could it be the wheat source of beer? Or its high-fructose corn syrup? I don't know, but beer is the least desirable form of alcohol of the choices we have.


Following these simple steps, it is unusual in my experience that you cannot achieve a triglyceride level <60 mg/dl. Rarely do we need to add fibrate drugs or other prescription agents to reduce triglycerides.



Copyright 2008 William Davis, MD

High-dose fish oil for Lp(a)

Lipoprotein(a), or Lp(a), is a problem area in coronary plaque reversal.

While our current Track Your Plaque record holder for largest percentage reduction in heart scan score has Lp(a), it remains among the more troublesome lipoprotein patterns.

One unique treatment for Lp(a) is high-dose omega-3 fatty acids from fish oil. While the data are relatively meager, there is one solid study from Lp(a) expert, Dr. Santica Marcovina of the University of Washington, called "The Lugalawa Study."

In this unique set of observations, 1300 members of a Bantu tribe living in Tanzania were studied. What made this population unusual is the fact that two groups of Bantus lived under different circumstances. One group lived on Nyasa Lake (3rd largest lake in Africa and reputed to have the greatest number of species of fish of any lake in the world) and ate large quantities of freshwater fish providing up to 500 mg of omega-3s, EPA and DHA, per day. Another Bantu group lived away from the lake as farmers, eating a pure vegetarian diet without fish.

Nyasa Lake












This situation among genetically similar stock provided a unique learning opportunity, a chance to assess whether different diets influenced Lp(a) levels.

The results: The fish-eating Bantus had an average Lp(a) level of 14.0 mg/dl. The farming, non-fish eating Bantus had an average Lp(a) of 27.0--a 48% difference. Curiously, a comparison of the apo(a) component of Lp(a) between the groups also showed that the fisherman expressed fewer dangerous small apo(a) forms, despite equal potential to express both.

The Lugalawa Study opens the question of whether similar results can be obtained not by moving to Tanzania and fishing Nyasa Lake, but by mimicking their experience by supplementing high doses of omega-3 fatty acids.

It's an intriguing question. In the Track Your Plaque program, we have no specific experience with this strategy, but it is certainly worth exploring further.

Watch for two upcoming Special Reports on the Track Your Plaque website in which we will be detailing 1)unique strategies for Lp(a) reduction, and 2) the usefulness of high-dose fish oil for coronary plaque reversal.

Interesting enough for a Virtual Clinical Trial?


Image courtesy Wikipedia.


Copyright 2008 William Davis, MD

The many faces of LDL

Pam has an LDL cholesterol of 144 mg/dl.

To most people, this means that she has a mildly elevated LDL value. Many people would respond by cutting the saturated fat in their diet. Most physicians would concur and talk about prescribing a statin drug.

Let me tell you what an LDL cholesterol of 144 mg/dl means to me:

1) It could mean an LDL of all large particles (which is good) or an LDL of all small particles (which is very bad). Or, perhaps it's some combination of big and small. I can't tell which just by knowing that LDL is 144.

Small LDL responds to a diet reduced in processed carbohydrates and wheat flour; large LDL does not. Small LDL responds in an exagerrated way to niacin; large LDL does not. It makes a difference.

2) It could mean that, hidden within LDL, is lipoprotein(a), or Lp(a). Recall that Lp(a) is a high-risk genetic pattern that can provide the false appearance of high LDL cholesterol. If Pam were prescribed a statin drug, it would have little effect and little benefit. (See Red flags for Lipoprotein(a).)

Knowing that Pam has Lp(a) can point us in an entirely different direction than just LDL cholesterol. It might mean high-dose fish oil, a more serious approach to niacin, hormonal treatments like DHEA or testosterone. It might mean more attention to warning your children about the possibility that they, too, might share this genetic trait.

3) It could mean both small LDL and Lp(a) are present simultaneously, an especially dangerous combined pattern that is among the highest risks for heart disease known.

4) Because Pam's LDL of 144 mg/dl was not measured, but calculated, it means that it is subject to tremendous inaccuracy.

In my office, calculated LDL cholesterols can be inaccurate by 50 or 100 mg/dl--commonly. So Pam's LDL of 144 mg/dl could really be 70 mg/dl, or it could be 244 mg/dl. Once again, it's a big difference.


Just like The Three Faces of Eve, the 1957 film in which Joanne Woodward played the three wildly different sides of Eve's personality--the daytime Eve White, the fun-loving and daring Eve Black, and Jane--so can LDL assume several different faces, all with different personalities, different implications.

Accepting LDL cholesterol as LDL cholesterol is a fool's game. It is only a starting point, nothing more. Accepting a statin drug based on LDL is, likewise, a trap fraught with uncertainty, the potential for limited or ineffective results, the price being your heart and health.
All posts by william-davis

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

You've come a long way, baby

In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.