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.

Drive-by angioplasty

Don had an angioplasty 6 months ago. When asked about the symptoms that prompted him to go to the hospital, he explained:

"I remember feeling really tired for about a week before I went. I'd read that fatigue can sometimes be a sign of heart disease. But then I had some trouble breathing. You know, like not being able to get a deep breath."

"My wife and I were planning on going on vacation. So I wanted to be certain something wasn't going on in my heart. That's when my wife insisted that she take me to the hospital.

"I kind of remember going there and arriving in the emergency room, but then I don't remember anything. Next thing I know, I'm waking up in a hospital bed. My wife and kids were there, looking all concerned. They said that I just got two stents and that the doctor just barely saved my life."

Happy story, happy ending? Not quite.

I reviewed the angiograms made during Don's hospital stay. They did, indeed, show some plaque, but not anywhere close to the amount necessary to account for symptoms like fatigue or breathlessness. For symptoms like this to occur without physical exertion, say, at your desk or relaxing at home, a critical >90% blockage would be required.

The worst "blockage" Don had was 50% at most. The leap was made to connect his relatively vague symptoms with these "blockages," leading to the implantation of two stents.

This is not as uncommon as you think. Yes, the practice of cardiology can be a life of acute procedures, urgent situations, and crises. Unfortunately, some people with questionable need for these procedures also get swept up in the wave. Sometimes it's due simply to the doctor's need to do "something," nervous family waiting in the wings. Sometiems it's intellectual laziness: putting in two stents seems to satisfy many patients' needs to have something "fixed," even when symptoms like fatigue could be due to anemia, sleep deprivation, a thyroid disorder, or any other myriad conditions that require a diagnostic effort (otherwise known as thinking). And sometimes it's simply done with financial motives, since angiplasty and related procedures pay well.

I call this "drive-by angioplasty," the impulsive, poorly considered coronary procedure that really should never have happened. How often does this happen? What percentage of heart procedures fall into this category? There are no clear-cut estimates. There are crude attempts by independent agencies that have put the number of unnecessary heart catheterizations up to 20% of the total number performed. The proportion of angioplasty procedures, stents, etc. that are not necessary is a tougher number to pinpoint, given the uncertainties surrounding the indications for these procedures, physician judgment that factors into the decision-making process, and the fact that many decisions are made on a qualitative basis, not precise quantification.

In real life, I would put the proportion of flagrant drive-by procedures at no more than 10%. However, that is 10% of an enormous number. The annual cardiovascular healthcare bill is $400 billion. 10% of that is $40 billion--an unimaginable sum. It also adds up to tens of thousands of people per year needlessly subjected to procedures. Consider that 10,000 heart procedures were performed today alone.

Should we push for legislation to control how and when heart procedures are performed? I don't think so. Despite my criticisms of the status quo in heart care, I still favor the freedom and rapid development of a free-market approach. However, you as a healthcare consumer need to be armed with information. You don't go to the car dealer unarmed with information on prices and comparative performance of the car you want. You should do the same with health. Information is your weapon, your defense against becoming the victim of the next drive-by heart procedure.

"Heart Healthy" and other lies

"Bankers believe liquidation has run its course and advise purchases."

New York Times headline, Oct 30, 1929, at the start of the Great Depression.






"I did not have sexual relations with that woman, Ms Lewinsky."

Former President Bill Clinton at a Washington Press Conference, 1998.






"The third quarter is going to be great."

Enron CEO, Ken Lay, just before the company reported a $638 million third-quarter loss, triggering the company's collapse.




Should we add the following to the list?


Heart Healthy Bisquick





















Heart Healthy snacks according to the National Heart, Lung, and Blood Institute:

Animal crackers, devil's food cookies, fig and other fruit bars, ginger snaps, graham crackers, vanilla or lemon wafers

Angel food cake or other lowfat cakes

Low fat frozen yogurt, ice milk, fruit ices, sorbet, sherbet

Pudding (make it with fat free or 1% milk), gelatin desserts

Popcorn without butter or oil; pretzels, baked tortilla chips






67% digestible carbohydrates/sugars from corn syrup, sugar, raisins, and honey. Oh, yes . . . and it contains plant sterols.





"Heartzels are a healthy snack alternative for anyone wanting to control fat intake and add fiber to their diet," said Tracy LaRosiliere, a Frito-Lay vice president of marketing. "What better time for Frito-Lay to launch its first heart-healthy snack than during American Heart Month and just in time for Valentine's Day."

The relationship with the American Heart Association and the launch of Rold Gold Heartzels Pretzels is the latest move by Frito-Lay to continue its commitment to offering a wide variety of low-fat and better-for-you snacks nationally, which like the company's assortment of regular chips can be enjoyed as part of a healthy diet and lifestyle.

Calcium chaos


Imagine that I'm planning to build a wall of bricks. I start by throwing cement at a pile of bricks, hoping that it forms a nice, orderly brick wall.

Fat chance, you say.

I believe that is what appears to be emerging as the situation with calcium supplementation.

A recent study from New Zealand reported an experience with 1,471 postmenopausal women, mean age of 74 years, who were randomized to treatment with either calcium supplements or placebo. Calcium was supplied as calcium citrate (Citrical) to provide 1000 mg of (elemental) calcium per day (400 mg morning, 600 mg evening).

(Bolland MJ, Barber PA, Doughty RN et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Brit Med J BMJ, doi:10.1136/bmj.39440.525752.BE; published 15 January 2008)

Over 5 years, women taking calcium had twice the risk of having a heart attack compared with women taking the placebo; women taking calcium had a 47 percent higher risk of having any one of three "events" (heart attack, stroke or sudden death) than women in the placebo group.

The findings of this study run counter to what we've been telling people all these years: Calcium supplementation, usually taken to halt deteriorating bone health and osteoporosis, modestly reduces blood pressure, reduces LDL and raises HDL cholesterol. At first blush, we might thereby presume that it also reduces cardiovascular events.

This study suggests that calcium supplementation does not result in reduction of cardiovascular events, perhaps even increases risk.

Certainly, this new finding will serve to confuse the public even more than it is already, particularly when it comes to strategies that modify risk for heart attack. However, this may make more sense once we stop and think for a moment.

Calcium supplementation inarguably slows, occasionally halts, calcium resorption from bone (through suppression of parathyroid hormone). Calcium also accumulates as part of atherosclerotic plaque in coronary and other arteries.

How does oral calcium know where to go--bones, not arteries or kidneys, in addition to serving all its other crucial functions?

Keep in mind that, in many roles, calcium is passive, something that responds to control exerted by some other factor. Vitamin D is that factor. Vitamin D controls the absorption of calcium in the intestinal tract (calcium aborption quadruples when vitamin D is restored to normal), it controls whether calcium is deposited in bone or extracted from arteries. It is the master control over the fate of calcium. Calcium just goes along for the ride.

Bone and arterial health do indeed intersect via calcium, but not through calcium supplementation. Instead, the control exerted by vitamin D (and vitamin K2, another conversation) connects the seemingly unrelated processes.

At what calcium dose threshold do the benefits stop and the adverse effects begin? That remains unanswered, particularly in light of this new study. However, this study calls into serious question the wisdom of supplementing calcium at a dose of 1000 mg, particularly when taken without normalization of vitamin D.

Calcium is therefore emerging as an important player in artery health. But just taking calcium makes no more sense than our brick wall and cement analogy. You might regard vitamin D as the mason that skillfully lays down both brick and cement in a neat, orderly way.

Another big Track Your Plaque success story

Lorenzo is an 81-year old retired manufacturing engineer whose intial heart scan score in late 2006 was an alarming 1102.

Recall that, despite feeling well and having a normal stress test, Lorenzo was facing a heart attack and death risk that was as high as 25% per year without preventive action.

Lorenzo was moderately interested in the Track Your Plaque concepts. While not exactly the most highly motivated, he did see the rationale in our approach. But he came to us mostly because his primary care doctor told him to.

Nonetheless, one year later, he underwent another heart scan. His score: 588--a 46.6% drop in score, nearly cutting his plaque in half. While Lorenzo didn't set any new records in terms of percentage drop in score, he has reduced his score in real numbers more than anybody else before: a 514 point drop in score.

Lorenzo joins the ranks of our current record holders, Amy, with a 63% drop in heart scan score, and Neal with a 51% drop in score. Both of these Track Your Plaque record holders, while achieving larger percentage reductions in score, achieved less when viewed on an absolute number basis.

Now, breaking records is not necessary to succeed in the Track Your Plaque program or at heart disease reversal. Even 1% reversal is still a big success, certainly more than is achieved in conventional practice.

No special commitment was necessary in Lorenzo's case. All he required was a little of the right kind of information. I can tell what he didn't do: Lorenzo did not follow a low-fat American Heart Association diet, he did not take high-dose statin drug, he did not deprive himself of food, he did not exercise to extremes. He just applied some simple strategies from the Track Your Plaque program.

I play these sorts of games just to make a point and to show just what is possible. While the world of hospital procedures and emergency management of coronary disease marches on, we are quietly reversing the disease. Sometimes, we achieve results that even surprise ourselves.

Lorenzo's full story will be detailed in the February 2008 Track Your Plaque newsletter. If you are not yet a subscriber, you can sign up (without cost)here.


Copyright 2008 William Davis, MD
Low-carb is heart healthy

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.

Comments (88) -

  • Henk Poley

    1/4/2012 6:58:20 AM |

    You'd say with all these claims it should be doable to prove or disprove scientifically. Why is there so much controversy around food?

  • Might-o'chondri-AL

    1/4/2012 7:20:41 AM |

    Hi Dr. Davis,
          I want to thank you for educating me about lipid profiles and think the following data might show readers  how some of your ideas play out (all varied experimentation coincided with a daily high protein intake).

    Innocent  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

  • Janknitz

    1/4/2012 7:23:37 AM |

    Dr John McDougall is coming out with a new book called "the Starch Solution" which advocates  NO fat and Little protein and eating a minimum of 900 grams of starch each day.  In the 80's he had a local call in talk radio program and I remember callers saying they followed the diet religiously but their triglycerides were sky high. He would tell these callers to stop eating fruit. Not much left when you can't have fat, much protein, or fruit.  He'd also tell callers that giving your child cow's milk guaranteed them to have diabetes and advocated sweetened rice milk instead.

    I'd love to see a well-designed study comparing your approaches.  Just don't ask me to be a test subject for his approach.

  • Stephanie

    1/4/2012 12:38:53 PM |

    I find that I garner all the benefits you list from following this dietary approach with the exception of one -- better sleep.  When I reduce my carbohydrate count, my energy soars and I suffer from terrible insomnia.  I have read that your body adjusts in, but I have not found this to be the case personally.  After 10 days of little sleep, I do notice that my fasting blood sugars are up 10-15 points and concentration starts to suffer (as well as patience).

    Do you have any suggestions for battling low-carb induced insomnia?  If I raise my carbs above 100, my sleep improves, but weight loss ceases (I still have more weight to lose) and blood sugar creeps a little.  I have tried herb teas and melatonin without success.

    Thanks for all you do!

  • Bill

    1/4/2012 1:01:55 PM |

    Dr. Davis, I'm curious what you make of the research showing big inconsistencies in reported LDL particle size between the various advanced lipoprotein analysis techniques. VAP, for example, apparently reports far fewer people as Pattern A than NMR, GGE, or TGE. Even measured LDL-C seems to vary quite a lot between the techniques.

    This seems to call into question the usefulness of such testing, since the results seem to depend mostly on which methodology happens to be chosen. Here's one example that has full text publicly available:

    http://www.clinchem.org/content/52/9/1722.full#_jmp0_

  • JC

    1/4/2012 1:43:55 PM |

    Can you comment on "Forks Over Knives"?

  • Jackie

    1/4/2012 1:46:27 PM |

    Dr. Davis,

    My husband, a patient of yours, has been following the no wheat diet for around 2 months. He also has been limiting his  carbohydrates to around 15 grams per meal.  He runs around 20 miles a week plus bikes around 30 miles a week. He has lost around 20 pounds in the last 2 months. He started at around 160 pounds..... I think he has lost way too much weight for his 6 foot frame. He says, he's just following your guidelines.

    Shouldn't athletes take in more carbohydrates than 15 grams per meal?

    Jackie

  • Todd B

    1/4/2012 2:47:40 PM |

    JC, Dr. Davis can speak for himself; however, if you are looking for a good critique/review of Forks Over Knives, I would recommend this one by Denise Minger:
    http://rawfoodsos.com/2011/09/22/forks-over-knives-is-the-science-legit-a-review-and-critique/

  • Joe

    1/4/2012 4:48:11 PM |

    Jackie, that gives your husband a BMI of 21.9, well within the "normal" range of 18.5 - 24.9.
    Your husband has transformed into a fat burner, and if he's able to continue working out at his current pace, I wouldn't worry about it.  But if he's lost muscle mass, or feels lethargic, he should probably up the carbs a bit, and the protein (perhaps a protein shake, post workouts?).

    A lot of people would love to have your husband's "problem."

  • lconnolly

    1/4/2012 5:18:46 PM |

    Mitochondrial
    Congratulations!
    There are alot of us at Track Your Plaque who are great fans of yours. Wish you would join us.

  • Gene K

    1/4/2012 6:46:19 PM |

    Having taken the same low-carb route and seen all the benefits Dr Davis lists here, I too had good sleep as my remaining frontier. I found the blog of Dr Kruse (http://jackkruse.com) a great addition to Dr Davis's program and a terrific education resource. Please read his sleep-related posts (http://jackkruse.com/category/sleep/) and all the rest for that matter, as all are related. I find it amazing how well these two view points (Dr Davis's and Dr Kruse's) agree. I made these steps to see my sleep improve dramatically: do not eat or exercise after 7:30pm, take a hot shower before bed, go to bed early enough to allow 7.5 hrs to sleep, wear an eye mask during sleep to ensure total darkness, take a capsule of lemon balm herb (Melissa) before bedtime.

  • Jackie

    1/4/2012 8:50:10 PM |

    I get a BMI of 19. On the website that I put in the calculations  it says he is "underweight".

  • Gene K

    1/4/2012 9:28:33 PM |

    And at the same time, the general public can read this: http://www.webmd.com/diet/news/20120104/report-looks-at-best-diets-easiest-to-follow. No comments...

  • Joe

    1/4/2012 10:18:06 PM |

    Jackie, I think I misread your message. I thought he was currently 160 pounds, and apparently he's lost 20 of those pounds, right? If so, this BMI calculator still has him within the "normal" range.

    http://www.cdc.gov/healthyweight/assessing/bmi/

        Underweight = <18.5
        Normal weight = 18.5–24.9
        Overweight = 25–29.9
        Obesity = BMI of 30 or greater

    Anyway, I'd say he's just fine, with the same caveats.  That is, if he's lost muscle mass, eat more protein (especially protein shakes after each workout), and maybe up the carbs a bit if he's feeling weak in any way. I ran the numbers on several other web sites (Mayo Clinic and NIH) and they all say the same. He's within the "normal" range, but just barely.

  • Judy B

    1/4/2012 11:04:28 PM |

    Stephanie,  I found that low carb gave me better sleep except when I took some supplements, etc, at bed time.  Don't know what you are taking, but I found that D3 at night kept me up and recently a new formulation of glucosamine (sp?) did the same (can't figure out what is causing that).  Soo, if you are taking anything in the late afternoon or evening, you might want to experiment and see if taking them earlier helps... Check Seth Roberts for info on D3 scheduling.

  • Might-o'chondri-AL

    1/5/2012 1:16:29 AM |

    Hi Jackie,
    I'm with you on 160 lbs. for 6 footer is too scrawny if the person is healthy . That is also my situation (being  6 feet tall)  if I go  low carb of  (say) fewer than 100 grams carbs daily .There is no current science that  adults being real thin is better than being heavier - just the opposite.
    When I get scrawny there's muscle, but my capacity for day in and day out sustained life style physical exertion is (in my 60 year old body) less than when I weigh more. And a day or two of  missing a good meal & exceptional stress
    or exertion can cause notable dip in weight when I'm eating very low carb.
    Doc has your husband as his  patient,  so there may be other considerations they are considering. I don't wish to confuse BMI with crucial medical goals they are working on. So am speaking of my own monitoring and my lab results (detailed above) are not necessarily what other slim individuals would see.
    I have not tried a months long protracted experiment of  gorging on more dietary fat as an alternative to my eating moderate daily carbs (say,  over 100 grams). Handfuls and handfuls of nuts don't seem to promptly boost me back towards 165 lbs. like augmenting with moderate carbs does.

  • PeggyC

    1/5/2012 4:16:16 AM |

    Stephanie, have you tried Magnesium citrate about an hour before going to bed?  It tends to relax you and help you sleep and it doesn't hurt--Magnesium is one of the one of the things we tend to lose on low carb. I take it to prevent leg cramps and it also helps me get to sleep.

  • PeggyC

    1/5/2012 4:19:59 AM |

    JC, Here is an excellent commentary on Forks over Knives: http://rawfoodsos.com/2011/09/22/forks-over-knives-is-the-science-legit-a-review-and-critique/ I'm sure Dr. Davis will concur with her analysis, though I will let him speak for himself on that.  However, in the mean time, if you haven't checked it out, Denise Minger does a great job of dissecting it.

  • PeggyC

    1/5/2012 6:24:58 AM |

    All I can do is sputter, sputter, sputter.  Talk about ridiculous!  The "diabetes diet" will ensure that a person stays diabetic and dependent on medication.  The "most heart healthy diets" will more than likely cause heart disease rather than prevent it.   The DASH diet also ensures that a person maintains high blood pressure and dependent on medication.  Awful.  But you're right--that's what the general public sees and believes.  Makes me wonder if there is hope.

  • Might-o'chondri-AL

    1/5/2012 8:59:28 AM |

    For Iconnolly & others,
    Doc  has everyone confused why he clinically finds wheat elimination more dramatic on gut fat than just restricting carbs. He decries modern dwarf wheat, yet not all genetic confabulations will have the same lectin protein structure, so this is details how some may play roles in adipose tissue changes. When a lectin has a molecular structure where their folded protein's usual strands coil like a loop, instead of just being strands, then what occupies the loop's center becomes important.

    If the peptide (protein building block) variation has an arginine amino acid leading that lectin's loop it can be a problem. That arginine torques the loop, makes it more flexible overall and gets where it is not supposed to be. It, this type of lectin variation, can itself be used in a pro-inflammatory way. It should be understood this lectin doesn't so much evilly abuse what it touched on the adipose cell as be acting more like a thing (substrate) involved in co-activation.

    Vascular adhesion protein 1 (VAP1) has a lesser known function as an enzyme (VAP1 = semi-carbazide sensitive amine oxidase) and it comes to the surface of adipocytes when there are immunological molecular action. Doc talks about belly fat being prone to inflammatory modulation and obese adipose cells can have macrophages crusting them. (The role of  vascular endothelium VAP1 is not discussed here.)

    On the adipocyte it's VAP1 (a folded glyco-protein molecule) is configured in a way that it's enzymatic function part is down a channel like groove with a leucine amino poking in that pathway sort of  like a goalie. This goalie leucine (Leu469 position) keeps random triggers from getting past it to tag upto where the actual VAP1 activation spot is and provoke stray responses.

    Franken-wheat, as per Doc's opinion,  with an arginine looped lectin can torque/slip past that VAP1 leucine goalie &  get to dock. If the genetic wheat leads with another amino at a lectin loop then it usually (can't say never, since maybe there is a rare amino lectin loop able to dock) basicly won't be able to navigate past the VAP1's  leu469 and engage catalytic action. And, looking at the other end,  there are likely individuals whose VAP1 engender a variation other than leu469 in the goalie placement that actually is less selective and lets some lectins without an arginine led loop slip down the alley to dock  and engage.Thus different world wide batchs of wheat and individual adipose tissue surface responses to lectins in general can vary, as we see.

    Once the franken-lectin with arginine docks into the adipose VAP1's activation center the enzyme  uses that lectin to perform a function. The vulnerable NH2 group of that lectin's arginine amino binds to that VAP1's  molecule called topa-quinone. Then a transitional enzymatic driven state (Schiff base) occurs and, as the Schiff base is not permanent, it segues into a kind of half way oxidation phase (for geeks the VAP1 amine oxidase oxidized the arginine's amine into an aldehyde with a byproduct of hydrogen peroxide, & some ammonium).

    Here, as a consequence of that modified oxidative change over, hydrogen peroxide (H2O2) is put out on the apidocyte cell in a generally speaking small amount. H2O2 is reactive but, it should be remembered,  also a signaling molecule in it's own right. Individual adipocyte conditions will dictate how some react and being gaseous H2O2 can penetrate cells and diffuse to play out it's roles . In general, H2O2  produced by enzymes outside/on the cell (as opposed to H2O2 generated inside cell cytosols or cell mitochondria) alters conditions setting things up for even more local immunological activity (most understand VAP1's classical adhesion function is to snag immune cell's rolling by in the circulation so they can get into a cell that is imperiled and use H2O2 to innately kill infectious agents).

    If one eats franken-wheat  with a lectin arginine loop and one's VAP1 leu469 gate-keeper is in place (to let it by) you still aren't absolutely doomed to an auto-immune like assault with  reactive H2O2 plaguing your adipose tissue. An unusual genetic quirk down in the  VAP1's enzyme activation site can have a variation of  the usual tyrosine amino in the 471 position (tyrosine471). Without tyrosine471 in the enzymatic well then no topa-quinone is made from  tyrosine and then instead the franken-lectin loop's arginine will just meet up with a phenylalanine molecule instead. And,  conveniently nice for those without topa-quinone down there in that VAP1 enzymatic site no Schiff reaction even starts to go forward &  so no H2O2 on the outside of  that adipose cell instigates the pro-inflammatory circumstances Doc traces back to wheat .

  • steve

    1/5/2012 3:33:27 PM |

    Might-O-Al:
    You said you take no meds, but Niacin at the doses you take would be viewed as a  med, and sexert powerful influence on lipids  in lowering them, and affecting the size of LDL particles.  It also increases the HDL.  I think you experienced all of this, so how much is from carb restriction vs

    Dr Davis:  From my reading it seems unclear that when you lower LDL particle count to say 800 or below, how important the mix is between large and small particles.  I believe this is even stated on the NMR report: "Small LDL-P and LDL size are associated with CVD risk, but not after LDL-P is taken into account".  I believe the writings of many lipidologists seems to say that at low levels of LDL Particles in line with your recommendations, the mix of small and large is not important.
    Might you elaborate on this?

    Thanks,

  • Might-o'chondri-AL

    1/5/2012 5:26:55 PM |

    Hi Steve,
    I don't think I am eating "low" carb - just not a naturally thin person eating unlimited carbs. In fact Doc, a fan of "very" low carb, seems to have been very tolerant of me here when elaborate any  contrarian comments.  I probably simply don't over-eat for my activity level.
    I did try Doc's suggestion to use the finger stick  home blood glucose meter to test how different carb amounts I was including in some of my experimental meals played out. And , putting  credence to his admonition about post prandial glucose "excursions" (spike), reduced some of my core meals' total carbs .
    In those examined daily staple meals (or thin me specifically)  I generally found I felt fine with the reduced carbs and the post prandial blood glucose tests examined at 15 minute intervals showed a more modulated excursion. But when I tried to go with very low carb (15 gr./meal) or even low carb (maybe barely 100 gr. daily) I became gaunt  (so apparently my  hold steady weight/strength is closer to  120 gr. carbs daily).
    I wanted last trial months to be less about precise control in home eating and more to see if modest dining out in the world (I usually work overseas & NMR test not available)  would adversely affect my lipo-protein fractions that Doc's other protocols (fish oil, niacin, vit. D, skip wheat) had started improving. I settled on cheap daily oriental restaurant lunch since cup of rice & fish/veggie cooked in vegetable oil  (with some sugared spice) is pretty much the best I have available to eat in developing countries.
    Agreed, that daily niacin of 2,000 mg is a self-dosing amount & yet is in Doc's upper range for unsupervised use (another practice I thank him for showing me here). To orientate any readers I'd like to be clear that  this is not to say I am blindly recommending such a high dosage.
    After 4 months on 1,500 mg. daily niacin I deliberately had some liver enzyme tests, SGOT (a.k.a. AST) & SGPT (a.k.a ALT), to make sure  I was not provoking unknown damage. When  taking 1,500 mg. daily niacin my  SGOT = 20 Iu/L (ideal = less than 40) & SGPT = 17 (ideal less than 55) makes me feel confident that the last 7 months of  taking 2,000 mg. daily niacin has also been safe, for me.

  • Joe

    1/5/2012 8:27:10 PM |

    @ Might: "There is no current science that adults being real thin is better than being heavier – just the opposite."

    Please define "real thin" and "heavier" and "gaunt" in clinically relevant terms.

    The BMI, while not perfect, provides a pretty good baseline.  In fact, the original studies included smokers (and artificially thin), which biased the results (of course smokers will have a higher mortality rate!) against the low side of "normal."

    "I’m with you on 160 lbs. for 6 footer is too scrawny if the person is healthy"

    I just don't understand a comment like that., Might.  If a person is, by definition, healthy, how or why can he be "too scrawny"?  By what measure?

  • jim

    1/5/2012 9:20:01 PM |

    Hi Might-o'chondri-AL,
    You must have a great job, I cannot afford the NMR so frequently. If you found a cheaper way to get that done, let us know ;)

  • steve

    1/5/2012 10:38:52 PM |

    Might O Al:
    Thanks for your detailed response.  Sounds like you have things under control.  How large are your LDL particles?  For me, mine seem to run on the low side- at 20.6 per NMR and without  very large carb restriction i generate lots of small LDL whether on low or high carb.  Not sure what is going on with the liver or the metabolic issue i might have.  Normal weight at 144 at 5'6", normal thyroid, D, so with a family history of CAD I take a statin and Zetia to control the level of my LDL particles which at last count were 560, but small of 400 with TRGS of only 52.   HDL of 55.  and HDL particles of 35.  Maybe a bit more fat will help the profile.

    From some of what i have read, as LDL particles get to a low level, size does not seem to matter. That is at least to Dr. Dayspring and others.
    Regards,

  • Ronnie

    1/6/2012 12:46:39 AM |

    I originally posted this question in the wrong place.  I know that low carb diets benefit all genotypes, but I've read that APOE 3/4's also need to consume LOW fat diets to lower their heart disease risk (as opposed to moderate fat diets for other genotypes).  Do you agree?

  • Might-o'chondri-AL

    1/6/2012 1:31:56 AM |

    Hi Steve,
    I am not a clinician & since seem endowed with good health  my concerns are different than Doc's patients. People here should remember this is Dr. Davis' blog & he has the cachet to give advice about real medical problems.
    As I've aged there are  physical changes I can detect and some research tells me are silently common. As a  6 foot 136 lb. high school wrestler I hit the mats as  "wiry". At 60, if  my 32 inch waist pants slip, I know  poolside that I look  like a "scrawny" old grey head instead of robustly fit.  
    My work in developing countries show(ed) me I was naturally like the under-privileged locals -  real thin on adequate food intake while working hard.  With age comes vulnerability, so without any body mass reserve (to draw down on) a whip thin "healthy" older person who develops an alarming health problem may (without competent intervention) have to catabolize their muscles for converting into survival energy ; the only thing is, that the aged (unlike the young) are also prone to sarcopenia (muscle loss) .
    I think all can see modern longevity is excellent,  and yet many are even overweight. A 2011 Cordoba Argentina study suggests their older overweight  women had better cognitive function than matched ones with normal BMI . Another  fairly recent report says that older overweight African-american women are more satisfied with their quality of life than matched American females of all  races.
    Doc told us he knows  tri-athalon  competitors who can't train to their satisfaction eating low carb. They would be good models for "health", but apparently they want some reserve -  for at least the upper body strength (all muscle isn't identical) .
    Sorry no precise numbers/definitions were given. If my shaving mirror shows a a tight face hinting at the underlying bones  then I'll eventually weigh myself.  When I get a couple of lbs. back over 160 lbs. I  see some softness in my face, stop looking like am  malnourished & seem to get less easily tapped out using my upper body muscles when life demands it.

  • Might-o'chondri-AL

    1/6/2012 1:53:59 AM |

    Hi Jim,
    $70 NMR online script, your local ( most states legal) blood draw service via iNeedLabs dot com -  not financialy associated. Doc's theories intrigued me .... Since usually am somewhat out in the bush, with rustic medical care, I decided to repeatedly cough up the test money when 1st NMR showed I was way off Doc's mark. I've an abysmal familial cardio-vascular  history that I'd already beat & now feel have a demonstrably (NMR tested) better protocol.

  • Might-o'chondri-AL

    1/6/2012 2:59:41 AM |

    Hi Steve,
    1st NMR (low fat, unmonitored carbs) LDL size = 20.6 (size)
    2nd NMR (up fat, mostly rice, less carbs) LDL "  = 21.1
    3rd NMR (more fat, more niacin, + carbs ) LDL" =   21.3
    (lab calls LDL size of  20.6 to 23 as "large" - so mine got  bigger).

    I don't know if what the doctor you mention is valid. Some investigators contend when LDL gets down to around 60 mg/dL (in that traditional measurement scheme) the conditions are such that LDL can (will?)  be drawn back out  from within the vascular wall intima; and so there is a  mitigation of the amount of cholesterol in that plaque. Maybe this is what Dr. Dayspring is alluding to & presumably the logic would follow that this reduces risk factor ; making LDL cholesterol particle size  irrelevant because even if it is smLDL & prone to cause problems it won't get to accumulate where it shouldn't to the degree it can cause real damage.
    I am not declaring the preceding to be a relevant fact, and have additional issues in light of the following nuance. A  Cochran Group (2009?) independent meta-analysis of years of statin research indcates  that although statins are demonstrably useful helping those who already have had a cardio-vascular event (and survived) the same statins are not statistically proving to prevent someone from having their first cardio-vascular crisis.
    Ideally Doc will address whether LDL particle size can be irrelevant & when.
      .

  • Stephanie

    1/6/2012 1:26:39 PM |

    It is the ketosis that gives me insomnia.  My supplements have been steady for a couple of years and my regimine includes magnesium citrate and citramate.  Does anyone else experience insomnia when in ketosis?  If so, have you found a way to combat it?

  • berger6696

    1/6/2012 3:47:33 PM |

    I really wish this would be addressed in more blog posts.  I will be getting my ApoE results in a few weeks and am highly confident I am not 3/3.   Possibly even 2/4.  Yikes!

  • Gene K

    1/6/2012 3:50:38 PM |

    You can find previous posts on this topic here: http://www.trackyourplaque.com/blog/category/apoprotein-e.

  • Sol y Sombra

    1/6/2012 4:40:20 PM |

    Stephanie, my personal experience is you do not have to be in ketosis to lose weight. Sure, it happens more slowly than while in ketosis, but it does happen. That is, if you keep your carbs between 50 and 100 grams a day (fiber included). What exactly do you mean by "weight loss ceases" - how many pounds do you have to lose and for how long have you plateaued? If it has been less than a month or two since you last saw any weight loss, I don't think you have any reasons to worry just yet. Give your body time to adjust. And maybe start exercising too - try high-intensity interval training and body weight exercises or weight lifting.

  • Joe

    1/6/2012 5:25:29 PM |

    "As a 6 foot 136 lb. high school wrestler I hit the mats as “wiry”. At 60, if my 32 inch waist pants slip, I know poolside that I look like a “scrawny” old grey head instead of robustly fit."

    Again, Might, you seem more concerned with appearance than with health or fitness. Which, of course, you're entitled to do. And so is Jackie. She thinks her husband looks better with 20 more pounds on his frame. Even though he is within the "normal" or "ideal" BMI range, a useful measure of overall health and mortality. That's a good place to be, in my opinion. So I don't see any reason for being concerned about it, which she seems to be (I could be wrong about that, too).

    And if you feel that you look better at the pool with a few more pounds on your own frame, by all means, go for it!

    PS: Just putting a few more pounds (especially if they're just pounds of fat) on your frame won't necessarily keep you from getting "tapped out" when using your upper body muscles, but lifting more weights, more frequently, will.

    PPS: I'd really like to see that study that says African American women are more satisfied with their quality of life than others. It just doesn't compute. Neither does the Cordoba Study, which is refuted by dozens of similar studies.

  • Sol y Sombra

    1/6/2012 5:48:26 PM |

    I'm sorry, you say that if you up your carbs to 100/day, the sleeping problem resolves, but weight loss stops. I think you can try to stick with 100, perhaps up to 120, give yourself time and see if things improve. Many people can lose weight while eating between 100 and 150 g/day.

  • Might-o'chondri-AL

    1/6/2012 7:18:56 PM |

    Hi Joe,
    J. Zilberman, MD, Instituto Cardiovascular de Buenos Aires, Argentina studied 300 post-menopausal Córdoba women, with 52.6 % having obese BMI,  administered Boston Abbreviated Test & Mini-Mental Statement Examination" to  put forth findings "Association Between Menopause, Obesity, and Cognitive Impairment" at Oct. 2011 U. Mississippi conference "Physiology of Cardiovascular Disease: Gender Disparities"  hosted by University of Mississippi  relating that, in +/- 60 year old females those having more BMI correlated with more cognition - including the stipulation that waist width due to obesity (in other words adjusting for limitations of using BMI) postitively, meaning yes in a good way, correlated  with over all cognition. The researchers only speculate the cause of  this female cognitive benefit is because fat holds estrogen ,and so the more fat the more post-menopausal estrogen availability to allay impairment.

    To be clear I am definitely not trying to imply overweight African-american women will have ideal physiological health, yet mental ease has it's benefits for quality of life. If you look at Japan health research you will also find categories beyond raw number measurements. Consider  2011 U. Alabama  report by team of  Dr. T. Cox "Examining the association between body mass index and weight related quality of life in black and white women";  DOI 10.1007/s11482-011-9160-8

    Politely, can I ask you your age?

  • yuma

    1/6/2012 7:45:00 PM |

    Hi Dr. Davis,
    you recommend 40-50 grams of carbohydrates per day, 13-16 per meal, assuming 3 meals per day.
    If I only had 2 meals per day (i.e. intermittent fasting) would I still have only 13-16 C per meal or 20-25?
    If I only had 1 meal per day (i.e. intermittent fasting) would I still have only 13-16 C per meal or 50?
    In other words, does the fasting period compensate for the impact of higher carbs per meal?

    Thanks!

  • TheArcher

    1/6/2012 8:31:52 PM |

    Greetings, Dr. Davis and Track Your Plaque readers,

    I’m a 57-year-old lady who just stopped eating wheat in pursuit of a 40-pound weight loss and more energy. My husband and I like many foods on a low-carb diet.  I don’t miss wheat at the moment, and my husband is coping okay wheatless; but he wonders, in the absence of bread, what he can use to sop up sauces, olive oil, etc. at dinnertime. Surely he’s not the only person who became accustomed to using bread this way.

    I can’t think of a grain-free low-carb substitute. Can anyone else suggest one?

  • steve

    1/6/2012 8:52:07 PM |

    Dr Davis:
    Can you clarify and give us your view as to how important LDL particle size is when total LDL particles are 600 or less?  Thanks.

  • Janknitz

    1/6/2012 9:22:37 PM |

    I miss bread for that particular reason too!   It's about the only time I really, really miss bread.  
    .  I use this recipe http://247lowcarbdiner.blogspot.com/2011/11/bacon-avocado-grilled-cheese-sliders-on.html?m=0 for the coconut "bread" and it's savory and does a good job sopping up all those delicious sauces.

  • Janknitz

    1/6/2012 9:29:16 PM |

    Just had my lipid panels done after about 7 months wheat free and low carb:

    Total Cholesterol:  235
    Triglycerides: 71
    HDL: 79
    LDL: 142 (calculated)
    Pretty darn good, though I'll keep working on getting the Triglycerides down even more.  I didn't have baseline numbers, but I suspect that they were really bad as I'm severely insulin resistant, obese, and was totally inactive before starting.  Insulin resistance is still not where I'd like it to be, but my HbA1C is not bad at 5.8.  All these numbers are 100% due to my wheat free, low carb diet, plus fish oil and Vitamin D3 supplementation.  I'm THRILLED.  

    Added bonus:.  Skeletal pain that was 7 on a scale of 10 every moment is GONE (doctor said it was aging).  Low back pain is gone, and I don't think it really left UNTIL I cut out the wheat.  GERD gone, asthma under the best control ever.  I can walk 2 miles now, I couldn't even walk across a room 6 months ago.  

    It works, it works, it works, it WORKS!

  • Joe

    1/6/2012 10:33:09 PM |

    This works for me:

    http://www.youtube.com/watch?v=DX7wrTX8ybQ

    Especially for soaking up egg yokes.

    It also tastes great when toasted, buried in butter and carb-free pancake syrup, with a little cinnamon sprinkled on top.

  • Joe

    1/6/2012 11:02:05 PM |

    Yes, Might, I found the study, and question the results, in light of so many studies that suggest just the opposite is true.  Additionally, it doesn't say anything about men.

    Regarding Alabama study? It concluded pretty much what I expected it to conclude, that "  obesity not only increases risk for morbidity/mortality, but also impacts the quality of life of obese individuals." Yes, I think African American women are more comfortable with obesity and being overweight (a cultural artifact?) than white women (which is probably why they are less healthy and suffer higher rates of mortality than white women), but you suggested this translated to a better "quality of life," and I don't think that's necessarily the case. Too much of a leap, I think.

    About my age?  Sure. Do you want my biological age? That would be 70. So I'm entering my eighth decade on this planet, and feel like I'm still in my 30s. That's mostly because I now look a lot like I did in my early 30s (less most of the hair!), while I was still smoking and still led an active, physical life. I'd rather not talk about my late 30s, 40s, 50s and early 60s, when the wheels came off, and before "I saw the light." Smile

  • Might-o'chondri-AL

    1/7/2012 3:21:42 AM |

    Kudos Joe,
    So you'll like this: in the pool the other day I met a fellow in his early 90's who eventually asks me my age. I tell him 60 & he deadpan's: "I got shoes older than you!"

  • TheArcher

    1/7/2012 8:23:42 AM |

    Thanks for sharing that link. I'll try it. I'll also post back any other solutions I may find.

  • TheArcher

    1/7/2012 8:24:47 AM |

    Many thanks for that, Joe, and also for the other serving suggestions. I'll gladly try it.

  • Might-o'chondri-AL

    1/7/2012 9:09:37 AM |

    Zero body fat is not ideal because healthy adipose tissue gives us adiponectin in circulation. In skeletal muscles adiponectin turns out to increase the skeletal muscle enzyme LPL (for geeks: adiponectin upregulates AMPK, which increases PGC-1alpha & also PPAR alpha leading to increased lipoprotein lipase). This essentially gives the enzymatic ability to break apart VLDL for freeing up some of the triglycerides VLDL carries to bring in it's fatty acids to "burn" in the skeletal muscle cell's  mitochondria for ATP.

    Healthy adipose sending out adiponectin can actually increase the number of mitochondria being made (mitochondrial bio-genesis response is from increased AMPK) and up the potential for "burning" fatty acid  in that muscle cell; this essentially lowers the amount of lipids in muscle tissue; so having some body fat can still help keep muscles mass lean.

    Doc has to oversimplify blogging about carbs and body fat, yet I like his gist. Here's why: high blood glucose causes an intermediate molecule (succinate,  & then it's derivations ) to form that blocks  +/- 25% of  adiponectin from forming  ideally ( in that adipose cell's endoplasmic reticulum). This is detrimental because then target skeletal muscle cells have to make do on less than 10% of  the ideal high molecular weight (HMW) adiponectin than those with healthy adipose get to work with.

    To phrase it simpler,  those whose carb derived blood glucose load is too much for their physiology end up living with a low level of   ideal (HMW) adiponectin (ex. those with metabolic syndrome, obese, type II diabetic). And then there's sparse skeletal muscle LPL  for setting up the steps to get maximal "burning" of one's fats in their skeletal muscle (ie: stamina suffers).

    But then it turns annoying since, as Doc warns, too high a blood glucose (from dietary carb load one can't use up) makes the liver get driven by the carbohydrate response element binding protein (ChREBP) to turn  those excess carbs into triglycerides. And furthermore,  that high level of ChREBP  put into play also causes the person's adipose fat cells to boost expression of  their specific adipose tissue LPL (ie: body switches off skeletal muscle LPL, but turns on adipose LPL). In this situation the result is a lot of  triglycerides end up getting shunted inside of the body's adipose fat tissue cells so fat cells swell.

    At the same time adipose tissue is sucking up triglycerides skeletal muscle LPL is (for the most part) not showing up to work. So most of the post-prandial made triglycerides the VLDL is trying to unload from circulation over to skeletal muscles for use can't be plucked in by their skeletal muscles. One way to look at elevated triglyceride lab results is it (high trigs) indicates that body's adipose tissue isn't forming adiponectin "normally" enough to perform out & about in the other parts of the body. Doc has specified that human body fat (adipose) isn't a victim that passively receives goops of fat, but rather an actor  - like how it should send adiponectin to help skeletal muscles.

  • Dr. William Davis

    1/7/2012 3:06:54 PM |

    Nicely done, Might!

    Your experience is a perfect example of what can be achieved with diet and some supplements--no drugs!

    The world has been persuaded that statin drugs are the only answer. Your experience shows that you can achieve values that are SUPERIOR to those achievable with drugs.

    I'm going to post your comment as blog post. Thank you!

  • Dr. William Davis

    1/7/2012 3:08:16 PM |

    Perhaps we should call it the "Don't eat anything diet," or the "Eat only vegetables diet."

    Dr. Jeff Volek and Dr. Ron Krauss are among the investigators who have already provided validation of these issues using lipoprotein analysis.

  • Deb

    1/7/2012 3:20:41 PM |

    I make the 2 min bread recipe using almond flour.  Basically, its
    1/4 c. almond flour, 1/4 tsp baking soda, 1/4 tsp baking powder, pinch of salt, 1 T oil, 2T heavy cream, and 1 egg.  I mix it in a small square pyrex and bake in the microwave for 2 min.  Then I slice it in half to make it thinner and toast it.  Voila!  It passes for bread and makes a great LC sandwich.  Something like this does make being LC and grain free, a whole lot easier!

  • Dr. William Davis

    1/7/2012 3:32:25 PM |

    I wonder if the circadian variation in cortisol is thrown off as you lose weight, e.g. evening surge rather than morning surge.

    Some people in this situation have had success with higher doses of melatonin, e.g., 10-20 mg and/or the Seriphos form of phosphatidylserine.

  • Dr. William Davis

    1/7/2012 3:35:41 PM |

    Yes, Denise Minger does a great job, citing issues that I would have cited, also.

    As always, nutritional thinking falls into this trap: If something or some practice that is bad is replaced with something less bad, then more of the less bad thing must be good. If the standard American diet is replaced with a plant-based, low-fat diet and there are apparent benefits, then this diet must be the ideal.

    False logic. And the notion that the diet advocated by Esselstyn et al reverses coronary disease is a fiction. This is a whole conversation in itself. Perhaps a topic for future!

  • DonOverEasy

    1/7/2012 3:37:14 PM |

    Dr. Davis,
    I have experience so many benefits since I've been following your dietary suggestions for over a year now.  My question is:  What do I say to the veggie-heads and Ornish followers who claim and ask the question:  If low fat diets really worsen the factors leading to heart disease, please explain why  rural China was so unaffected by heart disease in the 80s?  

    I'm not a scientist or a researcher, and I know low-carb sure works for me, but  how do I respond to this question?  I'd like to be able to provide an intelligent, straight-forward answer to this never-ending argument.   Thank You.

    www.amazon.com/review/R2W7KWZKQY6BGJ/ref=cm_cd_pg_pg128?ie=UTF8&cdForum=FxZJ813G2J60B7&cdPage=128&asin=1439190275&store=books&cdThread=TxCB0L17B0KXSQ#wasThisHelpful

  • Dr. William Davis

    1/7/2012 3:38:31 PM |

    Excellent points, Joe. Thank you.

    Also, note that this diet is not calorie-restricted. If you'd like a 3-egg omelet with mozzarella cheese, covered lavishly with olive oil, spinach, mushrooms, and green peppers, have it and go back for seconds.

    Some people who exercise for prolonged periods, however, may require additional carbohydrates, such as a banana or cooked sweet potato or glucose preparation (Goo) in the midst of exercise.

  • Dr. William Davis

    1/7/2012 3:42:51 PM |

    I pay no mind to what Liposcience says, as the data they use and the concepts followed for crafting "reference ranges" is flawed. I like their service (for the most part; they are quite dysfunctional when it comes to customer service), but I do not agree with some of their information.

    There's too much here to cover in a comment, so suffice it to say that we cannot craft "normal" or "desirable" ranges for endpoints based on cardiovascular events, since events will lag or underestimate what the disease itself is doing, i.e, a measure of atherosclerosis. Also, Liposcience often bases their observations, as do many lipidologists, on values within a population, e.g., calling "normal" the median +/- 2 standard deviations. This is a deeply flawed notion of "normal."

  • Dr. William Davis

    1/7/2012 3:43:42 PM |

    No, I do not.

    I believe the cut the fat notion for apo E4 is an oversimplification.

    Perhaps this is worth covering in future.

  • Dr. William Davis

    1/7/2012 3:44:38 PM |

    No, it does not.

    Hyperglycemia and glycation develops after a specific carbohydrate ingestion and has no "memory" for what was or was not consumed earlier.

  • Dr. William Davis

    1/7/2012 3:46:16 PM |

    I post recipes on both www.trackyourplaque.com and the Wheat Belly Blog that accompanies the Wheat Belly book: www.wheatbellyblog.com.

    There are also around 35 such recipes in the Wheat Belly book. The next Wheat Belly book, slated for release in early 2013, will contain 150-200 recipes.

  • Dr. William Davis

    1/7/2012 3:48:03 PM |

    Still important, Steve.

    Note that persistent small LDLs do not occur in isolation, but are often accompanied by postprandial lipoprotein distortions and higher levels of glycation. So persistent small LDL, regardless of the proportion to total LDL, serves as a marker for several metabolic distortions.

    Note that I do not track LDL particle size; I track number of small LDL particles, what I believe is a superior marker.

  • Dr. William Davis

    1/7/2012 3:49:40 PM |

    Excellent, Jank!

    Also, note that the calculated LDL likely overestimates the true value, a common situation as you get healthier. At some point, an NMR LDL particle number or an apo B will show you the real value and I'll bet it's much lower than the calculated value suggests.

    And that's great on the bony pains.

  • Dr. William Davis

    1/7/2012 3:50:54 PM |

    HI, Don--

    A topic for future.

    In the meantime, please be sure to read Denise Minger's reanalysis of the China Study data that essentially debunks the entire argument.

  • Dr. William Davis

    1/7/2012 3:53:39 PM |

    Yes, this is a big problem, Bill.

    None of the lipoprotein testing companies talk to each other, leaving us with variable cutoffs for defining 'pattern A" and "pattern B." And there are next to no data with cross-technology comparisons.

    Until that happens, I ignore the semi-arbitrary and often misleading "pattern A" and "pattern B." Instead, use the total small LDL particle value and divide by total LDL and this gives you proportion or percentage small LDL. On VAP, add LDL3 + LDL 4, then divide by "Real" LDL.

  • DonOverEasy

    1/7/2012 4:24:30 PM |

    Thx doc.  I'm looking forward to understanding this better.  My mind is simple...  low carb is either better or it isn't. I know it is for me...  but apparently some people, for whatever reason, thrive on grains and low fat.  Would love to be able to come up w an answer.  Thank u.   Don

  • Might-o'chondri-AL

    1/7/2012 8:10:40 PM |

    Hi DonOverEasy,
        Next time you want to discuss diet theories with your friends show them  that 4 Jan. data  of mine detailed way above.
    The 1st results were for my long  standing life style  (ie: decades of my adult life) of eating high whole grain & low fat to theoretically prevent cardio-vascular problems my family is prone to. I was  "thriving", decent weight, did hard work and never seriously sick  - so everybody said I was a model for healthy diet. I had no symptoms of any bad reaction to any grains, unlike some get.
        But, according to Doc's preventative cardiology practice I was unknowingly burdened with way too much small LDL, even though I didn't have other metabolic issues (ex: spooky triglyceride levels).  I wanted to think maybe the report print out got messed up.  
       Then show  the 2nd lab results for evidence of how the small LDL improved as an  example of when stop being fanatically low fat &  unlimited whole grain (carb). If they say it was not a fluke show them the even better 3rd lab results after 1/2 year eating yet a higher fat intake.
       Of course individuals will differ & so you should ask them for comparison data from their own  NMR  (Doc's preferred lipo-protein test).  If their small LDL is negligible on their low fat  & grain (carb) based diet then that person is probably that way because of genetics; but you'll never be able to prove that of course & good fortune for them.

  • DonOverEasy

    1/8/2012 1:25:39 AM |

    Hi Might-o'chondri-AL,
    Thank you for your time and your reply.  I don't doubt you or your numbers.  My story is similar.  My problem lies with the folks who say we are a minority.  

    They say we are a small percentage of pre-diabetics, who will naturally do well on low carb.  My opponents maintain the vast majority of people thrive on whole grains,  low fat, and high fiber, otherwise  rural China  would have been the "heart disease capitol of the world" in the 1980s.

    I'm aware of Denise Minger and how she has shed light on Dr. Campbell's deceptive studies.  And my own story and dietary changes have proven Dr. Campbell is blowing smoke.  Yet there is truth in that, China has subsisted for thousands of years on high grains and low fat.  Rural China did have a low rate of heart disease.  Why is that?

    There's got to be more to this story.  The vegans maintain Americans are obese not because of whole grains and low fat, but because of an addiction to simple carbohydrates and sugars.  Which truly is part of the problem.  But only part of the problem.  They believe simple carbs and saturated fats are what causes the inflammatory response that has contributed to the masses with heart disease, not whole wheat grains.

    So Al (I presume) I hear you, loud and clear.   I too thrive following a paleo way of life.  I've lose 40 lbs and have great numbers.  But are we the minority?  I became sick on a vegan diet back in the 80s (Ornish), but I have friends (more like acquaintences) who appear to be thriving on a vegan lifestyle.  Again... why is that?

    I continue to search for answers.  Thanks for taking the time.
    Don

  • Might-o'chondri-AL

    1/8/2012 2:33:30 AM |

    Hi Don,
    I worked in many rural developing countries worldwide (like yesteryear's China)  and the majority of the people have (had) no food security. So even if the grain bin was full they had to feed their extended family on the realistic minimum (except for seasonal boons, like edible insect time)  or risk absolute if ate all their seed grain when planting time rains hopefully came back on time .  
    In terms of your context this meant they did not overeat assorted types of calories in relation to how hard their daily physical exertion promptly used those available calories. We are not talking about people who are subsidized with food like the  modern societies make possible -   to put them into their actual context  they were (are) eating by the sweat of their brow. I think there is a blogosphere disconnect with only fasting being our link to subsistence level living;  &  to discard any relationship to "calories in, calories out"  as a sound bite just because modern food availability is pervasive..  
    Rural poor did (do) not eat all their livestock or fowl because it's their only source of  cash income at market and so made do with legumes (ex:beans & bushy pidgeon pea) . There is (was) no refrigeration so the vegetable & fruit crop diversification made it practical to just go with what held up reliably  (ex: cabbage) or grew fast (ex: leafy greens). Cooking traditions in rural cultures was not really an art but a means to conserve things from spoiling until got used (ex: fried makes a barrier, sugar preserves, vinegar  conserves, ferments drop pH dissuades bacteria).
    Rural China's low cardio-vascular disease , looked through Doc's paradigm,  is they never had enough shear over-load  of  inappropriately excessive blood sugar to drive the metabolic aberrations which generate the physical changes in lipids (small LDL , triglycerides) that are cardio-vascular culprits. Doc's blogging puts protein source and fat amounts as not a factor in heart related problems, just what we are taught to worry incorrectly about.
    Have your veganites take an NMR even if they are thin for show and tell.

  • Tim Dietz

    1/8/2012 5:43:22 PM |

    Hi Doc,

    I'm an APOE2/4 and would love to have you cover this subject in more detail.

    Thanks,
    Tim

  • edgar@raw food diet

    1/9/2012 4:07:42 AM |

    Hi Dr. Davis,

    Thank you for confirming that low carbohydrate intake can really reduce the risk of heart attack. I agree that 90% of the time drugs don't help, natural healing is the more better road to take. I will have to read this multiple times so that I can absorb --- this is really interesting.

  • Stacie

    1/10/2012 3:18:02 PM |

    Here is a conundrum maybe someone can help with.  My husband, with CAD, follows a low-carb diet.  Has lost 20-25 lbs, blood pressure is fantastic.  However,weight loss has stalled over the last year.  Triglycerides still too high (319), HDL still too low (38).  Low-carb really has not given him the great results I have been hoping for.  Any ideas?

  • Might-o'chondri-AL

    1/10/2012 9:14:45 PM |

    Hi Stacie,
    This is a sleepy thread by now so Iet me inform you that if you read Doc's  old posts I think you will find him repeatedly saying "...cut out wheat " , even if you are already low carb dieting. Look above to my  5 Jan. elaboration  written "For Iconnolly  ..." of how I suggest wheat may be a stumbling block ,  beyond  wheat just it being a carb.  It may motivate your man to give Doc's advice a try.
    Also,  I refer you to the previous post titled "Mocha Walnut Brownies" where 4 Jan. I wrote "For Laura ..."  in response to your guy's same slump. Please know that, despite my commenting alot,  I am not an authorized spokesman for Doc, nor am I a clinician or medical expert.

  • Stacie

    1/10/2012 9:46:44 PM |

    Hi AL:  

       Thanks for the reply,  We are wheat free, as well as grain free.  I did not understand the post about palmitate.  I think you are saying  to eat less of it.  Our doctor(fantastic low-carb doc)hjas recommended that my husband eat smaller portions of fat, and increase vegetable portion size.  He also has begun  K2, D3, and omega-3 supplementation.  His Apo E genotype is also not good (E2/E4).  I do not know anything about genotype, so do not know what it means.

  • Might-o'chondri-AL

    1/10/2012 11:34:54 PM |

    Hi Stacie,
    Doc tweaks fat intake down for ApoE4 individuals, your physician says smaller fat portions & I detailed why palmitic acid (palmitate) dietary fat comes to my mind to focus on for limiting. In conventional research high fat diets are used on mice to give them problems, like high triglycerides and insulin resistance and palmitate  often comes up as indirectly culpable .
    Since we are all designed to make our own palmitate those with genetic &/or food driven high triglycerides might do better just limiting dietary palmitate as much as possible. The desired amount of saturated fat can be obtained from coconut oil & adding more olive oil, due to it's high oleate fat content, will keep the palmitate benign.
    When one is ApoE2/E4 it means they make and use a type 2 & also type 4 variation of the molecule ApoE. Look at next post  "DIet is Superior to Drugs" & my 10 Jan. comment about triglycerides and ApoE  for  now; & use Doc's  search feature for his words.
    10 Jan.'s focus is on carbs & triglycerides relationship with ApoE. In your case just ignore the carb phase minutia & interject  your husband's high triglycerides into the overall dynamic laid out. People can have genetic influences on triglyceride levels & this seems to be what you must deal with.
    ApoE nuances  relationship with triglyceride coping suggests to me getting dietary fat without the palmitate found in meat/whole dairy. Of course that is hard to jibe with the nicer idea of eat all the meat you want; but maybe worth a trial.

  • Stacie

    1/11/2012 8:19:10 PM |

    Thank you Al.  I read those posts.  My understanding, then, is that  because  of the E2/E4, my husband is carb and fat sensitive.  Great combo!  I guess he is busted.  He hates coconut oil,  but olive oil is okay.  We will follow our doctor's advice, eat more vegetables and less meat.  I am also hoping the D3, K2, and fish oil will help.  Here is the bottom line for us:  We will do the best we can diet wise,  not worry or obsess about food, love each other, and above all, trust God.

  • Ronnie

    1/13/2012 12:30:49 AM |

    I've always been fit and thought I was keeping myself safe from heart disease with my 10 mg Zocor prescription for the past 8 years along with exercise and trying to eat somewhat "healthy"  (TC under 200 with the zocor, triglycerides and LDL's under 100 and HDL around 70; my weight is 109, female, age 60).  But my new doctor did NMR on me and I was shocked.  I found out that I'm APOE 3/4, my ApoB was 100 and LDL-P 1206, HDL 72, TR 115.  Since then I've added Slo Niacin (500 mg to start), my doctor upped my zocor to 20 mg (from what I've read, APOE 4's don't respond as well to statins except maybe for simvastatin), cut my carbs and fat intake.  My next NMR will be in March.  Meanwhile, I sort of feel that as an APOE 4 I'm doomed to some level of heart disease, regardless of my numbers.  I've always been a negative person anyway....can you help allay my fears?

  • Pamela Andrews

    1/13/2012 1:57:34 AM |

    Dr. Davis, After my doctor took me off glimeperide December 16, 2011 my blood sugars rebounded upward even though at the time I was low carb and avoiding wheat.  I never lost but ten to twelve pounds on the Wheat Belly diet but followed your advice anyway because the arthritis symptoms cleared up nicely and also because of so much cardiovascular heritage on my Dad's side of family.  Just this past week I called my doctor again because my blood sugars were very unsatisfactory (FBS of 170 in the morning and 209 between meals).  He allowed me to try just one half of one mg. of the glimeperide.  At about the same time I began to read about Dr. John McDougall on the internet and at first dismissed him but noticed that in his most recent book, the McDougall Plan for Rapid Weight Loss, 1995, he too warns readers to avoid all flour products, breads etc.  So, I have NOT returned to eating wheat but have started trying to avoid meat and fats for a while, just to see what would happen (I have never tried this before, to go without meat).  Some good news:  My fasting blood sugar in less than 72 hours has gone down to 114 and the chest pain and arrythmias have gone away.  Maybe I am sensitive to both carbohydrates AND meats/fats.  Decided to put this on this blog instead of Wheat Belly facebook or blog because of feeling like perhaps I am in a minority.

  • Gene K

    1/13/2012 5:14:37 AM |

    Ronnie,
    I will let Dr Davis answer your question, but I wanted to give you some good news. I am an APOE 3/4 and my family heart disease history is terrible. I started off with an OK lipid profile (according to my PCP; I was taking Lipitor), but my NMR turned out quite bad and getting worse over time. My calcium score at that time (February 2010) was 209. Thanks to Dr Davis, with the correctly tuned diet, supplement, and exercise program, I was able to bring my NMR indicators to a very favorable range, and my calcium score in September 2011 was 191 (10% reduction). And yes, I have to take statins (Crestor 10mg). I can provide more details, but just wanted to encourage you that you are not doomed, simply because you are an APOE 4, so please do not give up!

  • JC

    1/13/2012 1:24:55 PM |

    False logic. And the notion that the diet advocated by Esselstyn et al reverses coronary disease is a fiction. This is a whole conversation in itself. Perhaps a topic for future!

    I can't wait for that conversation.Very soon I hope.

  • Ronnie

    1/13/2012 10:50:45 PM |

    Thank you for that, Gene.  I still haven't gotten over the inital shock of finding out my genotype.  It surprised me because neither one of my parents have/had heart disease.  But my fraternal twin sister has CAD which I attributed to very poor diet and sedentary lifestyle.  I'm guessing she's also APOE 4. Thanks again.

  • Ronnie

    1/13/2012 10:54:05 PM |

    Also, Gene, whatever details you care to share would be helpful and appreciated. Ronnie

  • Gene K

    1/16/2012 3:34:12 AM |

    I described the diet, which took me from my worst NMR in November 2010, to a significant improvement in March 2011, and finally to an excellent NMR in September 2011 (small LDL #P less than 90 nmol/L) and a 10% reduction in my calcium score, in my comment at http://www.trackyourplaque.com/blog/2011/07/the-exception-to-low-carb.html#comment-23722. I followed this diet meticulously. I was taking 2400 mg (EPA+DPA) fish oil, 8000 iu vit D3, 675 mcg iodine in kelp tablets. Following Dr Davis's advice, after finding out in December 2011 that I was APOE 4,3, I added Niacine 500 mg and Crestor 10 mg (all doses are daily). I also significantly reduced plant oils in my diet. Today I am experimenting with my diet trying to add fats such as 100% baking chocolate and coconut oil. (Don't know the results yet.) I also walk for 1 hr every day (from home to train and back, and some during the lunch break) and exercise 3 days a week doing interval training (HIIT) for 20 min and following the slow burn strength resistance program.

  • Gene K

    1/16/2012 3:43:52 AM |

    Please read other comments to that post on 7/31/2011. Especially, pay attention to Dr Jack Kruse's comment. His blog at http://jackkruse.com/jacks-blog/ is very relevant, dense, insightful, and useful. I never miss his posts (nor do I Dr Davis's).

  • Ronnie

    1/16/2012 3:04:44 PM |

    Gene, thank you very much.  I plan to read everything this evening.  Congratulations on all your hard work and effort regarding diet, exercise and supplementation.  I do have a question regarding your fish oil.  In the NMR I received, the notes said that "one study demonstrated ApoE4 patients had a 15.9% increase in LDL cholesterol in response to fish oil.  This needs to be confirmed in a larger study".  Do you know anything about this?  I take 1000 mg fish oil daily.  Also, I have another question which shows my ignorance regarding all of this.  My NMR said I is am 3/4; you write you are 4,3.  Does the order of the numbers make any difference?  Thanks again.

  • Gene K

    1/16/2012 7:08:08 PM |

    Ronnie, I have no background in the medical field, so I am trying to limit the content of my posts to the links to sources from which I learned and the facts of my own experience. I would defer answers to Dr Davis or somebody else who knows.
    The spelling APOE 3,4 is purely mine and I don't know whether the order or punctuation have any meaning here. To me, it doesn't matter.
    To find out more about the fish oil, read earlier posts by Dr Davis here: http://www.trackyourplaque.com/blog/category/fish-oil. You can also find the following post by Dr Kruse (including the comments) useful: http://jackkruse.com/is-fish-oil-good-or-bad/.

  • Ronnie

    1/17/2012 3:33:59 AM |

    A lot of great information on this blog.  Thank you, Gene, for the links and Dr. Davis, for your response.

  • Clavis Panax

    1/28/2012 11:48:57 AM |

    Dr. Clavis Eraslan product without side effects by Panax, a vessel is completely natural bronchodilator.
    Plaque in blood vessels, fat layers and removes slag. Opens the way to vessel. Capillary blood circulation, prevents arteriosclerosis.

  • Bill

    8/15/2012 8:33:36 PM |

    Dr. Davis,
    I read about a Harvard medical study: "Low-carb diets linked to atherosclerosis and impaired blood vessel growth".
    http://news.harvard.edu/gazette/story/2009/08/low-carb-diets-linked-to-atherosclerosis-and-impaired-blood-vessel-growth/
    The article said, "...mice placed on a 12-week low-carbohydrate/high-protein diet showed a significant increase in atherosclerosis, ... The findings also showed that the diet led to an impaired ability to form new blood vessels in tissues deprived of blood flow, as might occur during a heart attack."
    I hope you will read this article and give your opinion about "how" they conducted their test.  
    Thanks

  • adam

    10/10/2012 8:53:33 PM |

    Does anyone know how to reach TYP member Gene K who posted on this thread?   I would like the  link to Gene's diet that he followed for Apoe3/4  but the link that was posted earlier does not work, if you are out there Gene, or anyone, please email me diet at

    dbm1st@airmail.net

    Regards

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