Do statin drugs reduce lipoprotein(a)?

Alex had lipoprotein(a), Lp(a), at a high level. With a heart scan score of 541 at age 53, treatment of this pattern would be crucial to his success.

Part of Alex's treatment program was niacin. However, Alex complained about the niacin "flush" to his primary care physician. So, his doctor told him to stop the niacin and replace it with a statin drug (Vytorin in this case).

Is this a satisfactory replacement? Do statin drugs reduce Lp(a)?

No, they do not. In fact, that's how I often meet people who have Lp(a): Their doctor will prescribe a statin drug for a high LDL cholesterol that results in a poor response. The patient will be told that statin drugs don't work for them. In reality, they have Lp(a) concealed in the LDL that makes the LDL resistant to treatment.

Lp(a) responds to a limited number of treatments, like niacin, testosterone, estrogen, and DHEA. But not to statin drugs.

Now, statin drugs may still pose a benefit through LDL reduction. But they do virtually nothing for the Lp(a) itself. Unfortunately, most practicing physicians rarely go any farther than Lipitor, Zocor, Vytorin, and the like.

If your doctor tries to shove a statin drug on you as a treatment for Lp(a), put up a fight. Voice your objections that statins do not reduce Lp(a).

Breakfast cereals and toilet paper



















(Image courtesy of Brandon Blinkenberg and Wikipedia.)


What do breakfast cereals and toilet paper have in common?

You guessed it: They both belong in the toilet.

If you would like some insight into why your friends and neighbors have protruding bellies that conceal any glimpse of their toes, have to conduct that peculiar side-to-side gait that now characterizes many Americans' walking style, and are pre-diabetic or diabetic, look no further than your supermarket cereal aisle.

The Fanatic Cook has some particularly biting comments about this strangely American phenomenon at http://fanaticcook.blogspot.com.

Breakfast cereals range in quality from awful to bad. I don't know of any that fit into the Track Your Plaque program that aims to eliminate the risk of heart disease.

Another lipoprotein hurdle

A number of our Track Your Plaque Members have encountered unexpected difficulty obtaining the 2nd page of their NMR Lipoprofile lipoprotein results when their blood was drawn in a LabCorp laboratory. This is the page that displays the lipoprotein subclasses in graphic format: VLDL, IDL, LDL, and HDL subclasses.

If you are unable to view page 2, you're stuck with the averaged values displayed on page 1. In my view, page 1 is is a drastically "watered down" version that sacrifices some crucial information, particularly if you use NMR lipoprotein analysis in a serial fashion, comparing one study to the next over time.

Why would LabCorp do this? The response I received from a Mr. Theo McCormick, Director of Marketing at LabCorp, was some corporate-speak about . . . Actually, I'm not sure what he was saying. (Members can read the complete Track Your Plaque conversation in the Forum.)

In my view, withholding this information is none of their business. If you or your insurance company paid for the test, then the information is yours to view. This would be like saying that "Sure you paid for the blood test, but we decided that you really won't know what to do with it, so we're keeping it from you."

Please send your objections to the contact info below. Several of the Members who have participated in the Track Your Plaque Forum conversation have already done so. It can only help to add to the growing objections to this silly and unfair practice.

Alternatively, just boycott any laboratory associated with LabCorp. If they are capable of such ridiculous withholding of information, who knows what else these people do?


Contact info:


Theo McCormick, Director of Marketing
Laboratory Corporation of America
1904 Alexander Drive
Research Triangle Park, NC 27709
Phone 919-572-7454 (Direct)
919-361-7700 Main
Fax 919-361-7149
theo_mccormick@labcorp.com

Until we hear about some real action from them, please DO NOT USE ANY LABCORP LABORATORY.

More on aortic valve disease and vitamin D

I hope I'm not getting my hopes up prematurely, but I believe that I've seen it once again: Dramatic reversal of aortic valve disease.

This 64-year old man came to me because of a heart scan score of 212. Jack proved to have small LDL, lipoprotein(a), and pre-diabetes. But there was a wrench in the works: Because of a new murmur, we obtain an echocardiogram that revealed a mildly stiff ("stenotic") aortic valve, one of the heart valves within the heart that can develop abnormal stiffness with time.

You can think of aortic valve disease as something like arthritis--a phenomenon of "wear and tear" that progresses over time, but doesn't just go away. In fact, the usual history is that, once detected, we expect it to get worse over the next few years. The stiff aortic valve eventually causes symptoms like chest pains, breathlessness, lightheadedness, and in very severe cases, passing out. For this reason, when symptoms appear, most cardiologists recommend surgical aortic valve replacement with a mechanical or a bio-prosthetic ("pig") valve.

Now, Jack's first aortic valve area (the parameter we follow by echocardiogram representing the effective area of the valve opening when viewed end on) was 1.6 cm2. A year later: 1.4 cm2. One year later again: 1.1 cm2.

In other words, progressive deterioration and a shrinking valve area. Most people begin to develop symptoms when they drop below 1.0 cm2.

Resigned to a new valve sometime in the next year or two, Jack underwent yet another echocardiogram: Valve area 1.8 cm2.

Is this for real? I had Jack come into the office. Lo and behold, to my shock and amazement, the prominent heart murmur he had all along was now barely audible.

I'm quite excited. However, it remains too early to get carried away. I've now seen this in a handful of people, all with aortic valve disease.

Aortic valve stenosis is generally regarded as a progressive disease that must eventually be corrected with surgery--period. The only other strategy that has proven to be of any benefit is Crestor 40 mg per day, an intolerable dose in my experience.

If the vitamin D effect on aortic valve disease proves consistent in future, even in a percentage of people, then hallelujah! We will be tracking this experience in future.

"How often do you call an ambulance?"

I asked one of the CT technologists at Milwaukee Heart Scan what quesetions are often asked by people undergoing their first CT heart scan.

"That's easy," she said. " 'How often do you call an ambulance?' "

She went on. "People are very scared when they have their heart scan. In fact, some people don't even want to see their heart scan images and don't want to know their score--even after they paid $200 for the scan!"

I think she's right. People often remember the headlines that some heart scan centers have used: "Heart scan saved so and so's life!," when a high score led to a heart catheterization, stents, or bypass surgery. It's the sort of headline that gives people the impression that ambulances pull up to the scan center whenever a score is high.

So, how often is an ambulance called to the scan center? Never. Not once. A CT heart scan score is NEVER an emergency.

Emergencies occur in other places when people can't breathe, or are having pain in their chest, or pass out, emergencies that should not take anyone to a heart scan center. When heart scans are used properly, it is the person without symptoms who undergoes a scan to look for hidden heart disease. This cannot lead to an emergency.

Of course, that doesn't mean that a high score shouldn't prompt quick action in the next few days or weeks, like seeing your doctor to discuss the results, undergoing a stress test, discussing how to stop the score from progressing.

But call an ambulance? Forget about it.

If you are contemplating a scan but are scared that it could lead to a 911 call, don't let that stop you. But, in the event that you go to an unscrupulous center or get bad information, be sure to be armed with the best information possible. One good start would be to take look at our free downloadable book, What does my heart scan show? available for free on the www.cureality.com website.

Oat vs. wheat

Here's a fascinating 2002 study by Dr. Brenda Davy and colleagues at Colorado State University that examined the NMR lipoprotein differences between a diet enriched in oats and one enriched with wheat. (Davy BM, Davy KP, Ho RC et al. High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men. Am J Clin Nutr 2002; 76:351-358.)

36 sedentary, overweight men (average BMI around 30--obese), aged 50-75 years, were given a diet enriched with either oat bran (as oatmeal and oat bran, providing 5.5 grams of beta-glucan) or wheat (as a hot cereal or Frosted Mini-Wheats), with equivalent calories in each group. All underwent baseline NMR lipoprotein analysis.

Three months later, there were no differences in "anthropometrics" like weight, waist size, or BMI (though there was a trend towards larger waistlines in the wheat group). The NMR lipoprotein analysis was repeated.



Comparison of the lipoprotein changes revealed:

--LDL cholesterol: Down 2.5% with oats, up 8.0% with wheat.

--LDL particle number: Down 5% with oats, up 14.2% with wheat.

--Small LDL: Down 17.3% with oats, up 60.4% with wheat.

--Triglycerides: Down 7.6% with oats, up 22.0% with wheat.



The across-the-board differences between the wheat and oat effects were astounding. In particular, note the extraordinary effect on small LDL particles: wheat triggered a 60% increase.

Similar studies yielding similar results have been conducted elsewhere, including Dr. Ronald Krauss' group at University of California-Berkeley.

Now, this was a study conducted under the somewhat artificial circumstances of a study. But imagine this sort of habitual intake continues, not for just three months, but for years. After all, wheat has expanded and metastasized to all three meals, snacks, every day, 7 days a week in most Americans' diet.

What a wonderfully graphic representation of the undesirable effects of wheat products. When you see Mini-Wheats, Shredded Wheat, whole grain bread, whole wheat bread, whole wheat crackers, Raisin Bran, and the thousands of other wheat-containing products that promise health, run the other way. Grab some oat bran on the way out.

Vitamin D and autism

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

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




Vitamin D Newsletter


August, 2007



Dear Dr. Cannell:

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

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

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

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

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

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

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

Sincerely,
Paul, Washington, D.C.




Dear Paul:

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

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

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

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

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

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



Dear Dr. Cannell:

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

Susan, Toronto, Canada




Dear Susan:

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



Dear Dr. Cannell:

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

Emma, London, England.





Dear Emma:

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



Dear Dr. Cannell:

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

Mary, Trenton, New Jersey.




Dear Mary:

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

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

The Telegraph, Why is Vitamin D So Vital?

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

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

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

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

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

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

Michael Pollan Podcast

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

Author Michael Pollan: 'The Omnivore's Dilemma'

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

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

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

Are you addicted to fructose?

Try a little experiment:

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

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

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

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

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

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

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

Chicken Little

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

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

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

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

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

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

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

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

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

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

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

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

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

But beware of the media, acting as our Chicken Little, reporting on studies that prove nothing but only raise questions.
Why small LDL particles are the #1 cause of heart disease in the US

Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Comments (77) -

  • Bill

    9/15/2011 1:13:26 PM |

    But is there any real evidence that small LDL is a *cause* of heart disease? Correlation alone isn't sufficient, of course, and Chris Masterjohn has said that even the correlation largely disappears when traditional "risk factors" such as HDL, LDL, and triglycerides are added to the model.

    I ask in part because I am about to arm wrestle with my primary care doctor about my recent cholesterol panel:

    Total: 382
    HDL: 157
    LDL: 217 (calculated)
    Triglycerides: 39

    He's upset about the LDL, of course, especially since it's progressively risen over time (coinciding with dietary changes pretty compatible with TYP and including quite a bit of sat fat after years as a low-fat vegetarian). Naturally, he wants me to reduce my fat consumption and retest in four months, and I'm sure a statin drug recommendation will follow just as the sunset inevitably follows the sunrise.

    I am thinking of asking for a full lipoprotein panel, with the expectation that it will calm him down by showing 1) much lower real, measured LDL with my rock bottom triglycerides and 2) strong Pattern A LDL with my sky high HDL and low triglycerides.

    But I'm not certain if I can really make a convincing empirical case to him that Pattern A is benign with a high LDL. (I'm also hesitating after hearing Chris Masterjohn say that LDL particle size measurements are hugely dependent on the type of assay used and that as a result it's not clear what, biologically, any given result means until these methodological discrepancies are sorted out.)

  • Peter Silverman

    9/15/2011 2:41:59 PM |

    The article you cite says the number of LDL particles may be more important than the size.  Is that your experience?

  • Howard

    9/15/2011 3:02:31 PM |

    @Bill : Chris Masterjohn also mentioned in a recent podcast that the current measurement technology for LDL particle size is just not sufficiently accurate to be useful.

  • chuck

    9/15/2011 3:48:18 PM |

    what is your feeling on oxidized ldl?

  • chuck

    9/15/2011 3:52:16 PM |

    @howard
    yes, based on the hour to hour, day to day, week to week, and month to month natural fluctuations of lipids in the blood it is difficult to make any real judgements about cholesterol readings without doing multiple panels over a period of time.  the whole medical community seems to be screwed up in this respect.

  • Kathy

    9/15/2011 4:13:20 PM |

    I have no idea what Dr. Davis' response will be, but if you're interested in getting an NMR profile done on your own dime (and if there is a convenient location near you), check out directlabs.com for their September special.  An NMR profile will only set you back $79 (reg $127).  I've been waiting for this "sale" and am getting it done to show my own doctor.  Your health is ultimately in your hands - keep up the good fight!
    Best,
    Kathy

  • edward white

    9/15/2011 5:02:18 PM |

    Dr D,
    I totally agree small LDL is driven by excess carbohydrate intake and postprandial
    triglycerides. However there is a substantial subset of people whose small LDL
    is genetically driven. I believe you are aware of this phenomena.
    Please let these folks know what their options are to address this important issue!
    There can be a good deal of frustration when carbs and triglycerides are addressed but
    with little lowering of small LDL.
    Please help this substantial number of people out by outlining their options...
    Gib

  • Unix-Jedi

    9/15/2011 5:22:13 PM |

    Thanks for that information, Kathy.

  • cancerclasses

    9/15/2011 5:57:26 PM |

    It ain't good,  just ask Wikipedia.   From the Wiki page re 'Chronic endothelial injury hypothesis':
    "Once LDL accumulates in the subendothelial space, it tends to become modified or oxidized.[5] This oxidized LDL plays several key roles in furthering the course of the inflammatory process. It is chemotactic to monocytes; oxidized LDL causes endothelial cells to secrete molecules that cause monocytes to penetrate between the endothelial cells and accumulate in the intima.[6]

    Oxidized LDL promotes death of endothelial cells by augmenting apoptosis. Also, through the activation of collagenases, ox-LDL contributes to a process which may lead to the rupture of the fibrous plaque[7] Oxidized LDL decreases the availability of endothelial nitric oxide (NO), which, in turn, increases the adhesion of monocytes to the endothelium.[8] Moreover, NO is involved in paracrine signalling between the endothelium and the smooth muscle that maintains vascular tone; without it, the muscle will not relax, and the blood vessel remains constricted. Thus, oxidized LDL also contributes to the hypertension often seen with atherosclerosis."

  • Bob

    9/15/2011 6:12:21 PM |

    Test reply

  • cancerclasses

    9/15/2011 6:13:54 PM |

    Yes, French cardiologist Guy-Andre Pelouze MD. at the recent Ancestral Health Symposium said in his presentation "Paleodiet and atheroma: A Cardiovascular Surgeon’s Perspective" that:

    1. Native (the reduced form of) LDL cholesterol is NOT atherogenic, only the oxidized form leads to atheroma, atherogenesis & arterial plaque formation.

    2. Without oxidized cholesterol it's very difficult to have arterial plaque formation

    3. Anti-oxidants are ineffective in preventing atheroma.

    4. SDLDL easily enter the subendothelial space because SDLDL are less than 25 nm in diameter and the subendothelial space is 26 nm.

    5. Subendothelial space in humans is very different in humans than other mammals due to the large amount of smooth muscle in the arterial media below the the intima layer.

    And there's much more.  To see a video of Dr. Pelouze's presentation hosted on the Ancestral Health page at Vimeo just google 'vimeo, paleodiet and atheroma', then scroll to video number 33 in the right side box.

  • cancerclasses

    9/15/2011 6:42:38 PM |

    Do you REALLY believe that? We have the ability to measure the distance between the earth and the moon almost down to the millimeter, and certainly down to the centimeter. We have the ability to measure individual atoms with electron and other types of microscopy used in materials engineering and computer chip manufacturing.  Medical, biochemical & physiological textbooks are full of descriptions of the sizes of white and red blood cells, bacteria and viruses, etc. ad infinitum.  Do you REALLY think we lack the ability to measure SDLDL?  Don't be so ready to believe something just because somebody says something about it.  Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion.  

    Furthermore, what's the point of a statement like that?  Should we just give up measuring and trying to understand how SDLDL causes atheroma just because ONE guy says we can't measure them to his degree of satisfaction?  Should we just give up worrying about what we eat, and what we are being sold as foods that are arbitrarily declared to be safe to eat by some anonymous bureaucrat at the FDA?  Should we just ignore the ever increasing incidence rates of cancer, heart disease and atherosclerosis that by all applications of observation and simple logic are known to be entirely due to the modern industrial foods diet in every society and the peoples that subsist on them?  

    I don't think so.  Homey don't play that anymore, at least this one doesn't.

  • cancerclasses

    9/15/2011 6:55:16 PM |

    @Bill,  Google and see this study: 'Detection of low density lipoprotein particle fusion by proton nuclear magnetic resonance spectroscopy'.    
    "Abstract: Recent evidence suggests that fusion of low density lipoprotein (LDL) particles is a key process in the initial accumulation of lipid in the arterial intima. In order to gain a better understanding of this early event in the development of atherosclerosis, it would thus be necessary to characterize the process of LDL fusion in detail. Such studies, however, pose severe methodological difficulties, such as differentiation of particle fusion from aggregation. In this paper we describe the use of novel methodology, based on 1H NMR spectroscopy, to study lipoprotein particle fusion."

  • Don

    9/15/2011 7:24:04 PM |

    Bill,
    You have no worry since your triglycerides are quite low and therefore your LDL particles are of healthy size.  Your correctly calculated LDL is only 161 using the Iranian formula (used if triglycerides low).  See LDL calculator here:
    http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm

    And never use statins, just cut carbs.
    Don

  • cancerclasses

    9/15/2011 7:34:54 PM |

    "About 80% of cholesterol is composed of fats and oils (Current Atherosclerosis Reports 2004). The
    majority of an arterial clog, 55%, comes from defective cooking oils, containing mainly damaged omega 6. Most of us unknowingly purchase these oils in the cooking oil section of the supermarket. These are the oils we fry with and the oils added to most packaged foods; both fresh and frozen.

    Here’s another shocker. It’s not the saturated fat —it’s the adulterated omega-6 from food processing that clogs arteries! Contrary to what we have heard for decades, it is not the saturated fat you eat that clogs your arteries! How do we know this? A 1994 Lancet article reported investigating the components of arterial plaques. In an aortic artery clog, they found that there are over ten different compounds in arterial plaque, but NO saturated fat. This means the bacon, eggs, cheese, steak, whipped cream, etc. isn’t the reason for a clogged artery. These natural saturated fats are actually good for you. You need them for body structure.

    With the consumption and transport of defective processed oils, LDL cholesterol acts like a “poison delivery system,” bringing deadly transfats and other ruined oils  into the cells. It is primarily the oxidized (adulterated) omega-6 that clogs the arteries, NOT saturated fat!"  

    For more just google 'Brian Peskin saturated fat' and read the day away to your heart's content.

  • Jack Kronk

    9/15/2011 8:37:50 PM |

    "just because somebody says something about it. Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion. "

    lol. you must not know who CMast is.

  • cancerclasses

    9/15/2011 10:27:09 PM |

    Yeah, I do, and that's why I said that.

  • Dr. William Davis

    9/16/2011 2:40:13 AM |

    Hi, Gib--

    The strategies that reduce small LDL are the same whether it's genetically-driven or acquired. However, when (presumptively) genetically-driven, it's just harder and requires a more meticulous effort.

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern.

  • Dr. William Davis

    9/16/2011 2:42:32 AM |

    Big issue. Note that the real culprit in causing plaque may be glycated oxidized LDL.

  • Dr. William Davis

    9/16/2011 2:43:51 AM |

    Hi, Peter--

    No, I think that is wrong. It might be correct if small LDL is regarded in a dichotomous way, i.e., pattern A vs. pattern B. But, when viewed quantitatively, I believe the real culprit is quantity of small LDL.

  • Dr. William Davis

    9/16/2011 2:46:58 AM |

    No question: The various lipoprotein testing companies need to talk and standardize their definitions. But this does not invalidate the concepts.

    Chris Masterjohn is a very bright guy. But on this I disagree. I believe it is wrong to assume that triglycerides and HDL behave in perfect tandem with small LDL. While they do indeed correlate, they do not correlate perfectly and demonstrate independent behavior depending on postprandial phenomena and genetic factors like apo E and apo C.

  • Joyce

    9/16/2011 5:17:54 PM |

    This has nothing to do with LDL, but I don't know where else to ask this, so I'll dive right in.

    I am reading and enjoying your book Wheat Belly, but don't understand why you lump chia seed in with other non-gluten grains to avoid or minimize. .  In my mind it is closer to flax.  Chia is truly an oil-seed and not a grain according to Dr. Coates, the "father" of chia seed research.  I have used it generously, and feel it aids in weight loss.  Chia seed is high in protein and fiber and low in carbs.  Why are you telling us to avoid or limit it?  I feel it is healthier than flax even.

    Please, can you clarify your stance on chia?  I was very disappointed to read that in your book.  Other than that, I really enjoyed Wheat Belly, having avoided gluten for a few years now.

  • Joyce

    9/16/2011 5:33:17 PM |

    P.S.  According to calorieking.com website, 1 oz. raw chia contains 0 carbs and 1 oz. dried chia contains only 1 gram of useable carb.

  • Adriana

    9/17/2011 10:16:37 AM |

    Not everybody who has good HDL, good TG and eats a low carb paleo diet will have low small particle LDL numbers which is why an NMR LipoProfile is important.  People with gut issues, yeast issues,  H. Pylori or an otherwise compromised liver can have unhealthy LDL despite doing everything right on the diet front.  Getting to the root of these issues is critical to resolving it.

  • Dr. William Davis

    9/17/2011 1:23:49 PM |

    Thanks, Joyce. But I don't remember lumping chia with the bad stuff.

    In fact, as you point out, chia belongs with flaxseed as one of the few truly healthy, low-carb foods.

  • Joyce

    9/17/2011 1:45:31 PM |

    Dr. Davies, on p. 212 of your book, chia is lumped in with other non gluten grains.  Maybe in future editions, the publisher can remove that?

    Although I have been gluten free for years, my husband is finally going gluten free..ALL BECAUSE OF YOUR BOOK!  He has some health issues, so for that I humbly thank you.

    Also, his next Toastmasters speech will be on "Wheat Belly"...how about that!

    Thank you so much for a wonderful book.  Your recipes are awesome.  I look forward to a Wheat Belly cookbook!!!!

  • Linda

    9/17/2011 2:57:40 PM |

    There are so many well read and brilliant posters here that I am going to jump in and ask a question totally off topic. This is not Dr. Davis' area of expertise, so I hope others may help.
    I do believe I am dealing with a bone/heel spur. Too much treadmilling, trying to increase speed, etc. I have done research on the condition and I read that turmeric, taken 2-3 times a day, is helpful. I just recently began taking D3 as well, 5000 IU a day. Will the Vit D3 help as well?
    Any thoughts? No, I am choosing not to visit a doctor for a cortisone shot. I am using NSAIDS for the pain and that works very well.

  • nina

    9/17/2011 4:48:56 PM |

    I've just spotted this post.  Never tried chia and wonder what you thought.  Have your patients reported similar effects?

    Nina

  • steve

    9/17/2011 7:26:34 PM |

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern

    Could you go in to more depth as to what strict carb reduction menas?  Is it no more than 50grams of starchy carbs such as rice or potatoes, or 100Grams?  I am guessing it is individualized, but some range of restricitons with those who have been successful would be helpful.  
    I have always had a low level of Trigs- never higher tnah 75 even on a hi carb diet, and was surprised to find the NMR showing all small particles!  So Dr. Davis is right to say low Trgs not always indicative of having large LDL.  Switched to elimination of most carbs and totally changed the profile.  Only issue that is while i produced lots of particles with carb diet, i also produce lots of LDL particles with carb restriction.  Genetics i guess!  I am an ApoE 3/3, which was a surprise.  
    Thanks for the good work Dr. D.  Have gotten several to buy Wheat Belly.  It will have an impact!

  • Joyce

    9/17/2011 7:30:40 PM |

    Nina, I am not Dr. Davis (wish I had his knowlege!), and I hope he doesn't mind me jumping in here, but I leaned about chia a few years ago when I read a book by Dr. Wayne Coates on the subject.  Chia has definitely helped me lose weight.  It is very filling.  When mixed with fluids, the chia seeds expand, and they really help to fill you up.  I've found all sorts of wonderful chia recipes on the web - from Chia "Tapioca" to beverages, etc.  I mix  it into many foods.  I think it enhances their taste.  I feel the chia seeds help with weight loss because of their appetite suppressant potential.  I hope this helped, and my apology to the good doctor for hogging the thread.

  • PeteKl

    9/17/2011 10:24:07 PM |

    Your post doesn't provide a lot of info, but if I were to guess I would say your problem is more likely related to walking/running incorrectly than nutritional (assuming you are in reasonable physical condition).  The human foot wasn't designed to be encased in the heavily cushioned shoes we typically wear today.   As a result many of us don't know how to walk or run correctly.

    Some of the better shoe stores will video tape you on a treadmill.  Just seeing the tape may be enough for you to realize what you are doing wrong.  If that doesn't help, there are professionals who should be able to figure out what might be happening.  

    Also consider reading "Born to Run" if you haven't already (it's a good read even for non-runners).  It probably won't give you a direct solution, but it may give you some ideas on where to look.  Good luck.

  • Louise

    9/18/2011 2:10:34 AM |

    Dr. Davis,
       I am 56 and have a strong history of heart disease in my family. I have been eating low carb for a couple of years... ( around 60 gms carb per day average..no pasta, no potato, almost no grain)  My most recent lipid panel showed LDL of 140. HDL 81, Triglycerides 43, CRP 0.2. .  I requested a test to show size of LDL. My doctor declined to order this, saying all LDL is bad.  Instead I was sent for a heart scan  ( paid out of pocket) and my calcium score was 0.  
      So now I'm trying to lower my LDL by lowering saturated fat.  Hard to do when you eat low carb. I wonder if I might be one of those Apo E 4 types that you mention, so thought I should try,.
      Here are my questions:
         Can I test my LDL size myself, through a home test? Or should I try to find out if I have Apo E 4?
          Do I really need to lower LDL if my calcium score is 0?
    Louise

  • Bob Goldstein

    9/18/2011 4:02:36 AM |

    For the last year I have eaten zero fruit, zero grains, zero sugar. Have mostly eaten beef, occasionally eggs cooked in butter. Have done two VAP tests the last year. When I started a year ago, trigs were 115, now 142. HDL was 50, now 46. My LDL did show a change of going from pattern A/B to pattern A.
    Any ideas why a diet for a year devoid of fruit, sugar, grains, would show an increase in trigs, and a slight decrease in HDL. If I have Apo E4 would my ldl go from A/B to A.
    I have lost 25 lbs. in the past year. Could this be a reason my numbers seem to be off?
    Thanks,
    Bob

  • Dr. William Davis

    9/18/2011 3:44:29 PM |

    Hi, Bob--

    Yes, blood drawn in the midst of weight loss can be very misleading.

    Transient effects include increased triglycerides, reduced HDL, even much higher blood sugar. Thankfully, it all gets much better once weight plateaus for a couple of months.

  • Dr. William Davis

    9/18/2011 3:47:39 PM |

    Hi, Louise--

    Sad that you have to educate your doctor.

    I find it unacceptable that a nice person engaged in health is refused a simple, helpful test. Tell your doctor goodbye and find one willing to act as your partner and advocate in health, not an obstruction.

    Yes, you can test it yourself through services like PrivateMDLabs.com. My view is to 1) identify how much, if any small LDL there is, then 2) reduce small LDL with diet. If you have only large LDL, you will absolutely need an LDL particle number by NMR or an apoprotein B to know what the REAL value is.

  • Dr. William Davis

    9/18/2011 3:49:52 PM |

    Thanks, Steve.

    There are a number of posts on this blog that detail how to gauge individual carbohydrate sensitivity. The best way is to check 1-hour after-eating blood sugars. Second best: count carb with the cutoff being determined individually. Just go back over the past 6 months and you will find several discussions.

  • Dr. William Davis

    9/18/2011 3:51:17 PM |

    Hi, Joyce--

    Thank you!

    If chia is listed as among undesirable non-gluten grains, that was my error. Remember what Mark Twain said: "Don't read about health, else you might die of a typo."

  • nina

    9/18/2011 5:13:58 PM |

    Thanks for your response Joyce.  

    The part that fascinated me was the idea that chia triggers a drop in blood sugars without a pre-spike.  I can't find anything on the net about that and wondered if other people had similar experiences.

    Nina

  • Bob Goldstein

    9/18/2011 7:08:22 PM |

    Thanks for the reply Dr. Davis. I have a blood test scheduled six months from now, and hopefully I will see better numbers. My LDL shows pattern A so at least I did see one positive change.
    Love your blog. Have learned a lot and it was the reason I gave up grains and sugar. 1 full year, no cheats.

  • Annlee

    9/18/2011 10:41:56 PM |

    Consider also going barefoot as much as possible - around the house, etc. You don't necessarily have to run barefoot (unless you work into it *gradually* and choose to continue it). I've recovered from heel spurs with stretching my achilles, with emphasis on stretching the soleus, and letting my feet bear my weight without any props underneath. For stretches, Anderson & Anderson have a very good book - Stretching - available on amazon.com. You didn't develop the spurs overnight, and they won't clear that quickly, either. Be patient and work with your body.

    You may also wish to consider vitamin K2, very good for ensuring calcium deposition occurs in the correct locations.

  • Kira

    9/19/2011 6:52:43 AM |

    Hi Doctor Davis, I talked to your about a year ago and you were kind enough then to comment on my blood results saying there was nothing to worry about - according to the Iranian formula.  I would greatly appreciate if you looked at my new results, they scared my whole family, I certainly am not going to show to the family physician, and I don't even want to think about changing from paleo style of eating to some kind of low fat cholesterol lowering diet, and taking any drugs/supplements. But may be I have to? I am 36 y.o., 5'4 and weigh 104lb.
    Glucose 85
    VAP TEST:
    Lipids
    LDL Cholesterol 149!
    HDL 130
    VLDL 14
    CHOLESTEROL, Total 293!
    Triglycerides 48
    Non HDL Col (LDL+VLDL) 163!
    apoB100-calc 96
    IDL Cholest 4
    Remnant Lipo. (IDL+VLDL3) 12
    Sub-Class Information:
    HDL-2  35
    HDL-3  95
    VLDL-3  8
    LDL1 Pattern A 3.1
    LDL2 Pattern A 26.0
    LDL3 Pattern B  71.0
    LDL 4 Pattern B  31.4

    The ordinary, non-VAP Lipid panel shows:
    Cholest TOTAL 279 !
    Triglycerides 48
    HDL Cholest 144
    VLDL Cholest Cal 10
    LDL Cholest Calc 125 !

    Also, I can't understand how my vit. D can be so low - 29.0, when I have been sun tanning all summer here in Orange County, California, at peak hours. Is there anything that you know of that may inhibit the vit. D conversion from the sun?
    Again, I greatly appreciate any insight that you can give me on this situation...

  • Louise

    9/19/2011 4:52:38 PM |

    Dr Davis,
      Thank you for your reply.  For now, I found a lab I can go to and get myself tested. Two hours away.. (Oddly, I must leave NY state to get this done due to billing law.). I'm going to do this! Do you agree that my best choice is the NMR?

  • otterotter

    9/19/2011 5:43:51 PM |

    Hi Gib,

    Option 1 will be cutting the saturated fat and cholesterol from the diet in addition to cutting the carbs. I tried eliminating eggs and cheese and my total cholesterol down from 400 to 260. By adding back "one egg a day", it went back to 320 (that's the impact of the dietary cholesterol on me, confirmed twice). I am currrently trying to replacing all saturated fat with mono unsaturated fat (olive+canola), just want to see how big the impact is. I am also going to test coconut oil separately, it is a cholesterol-free plant based medium-chain saturated fat, there is a chance I might respond to it differently.

    Option 2 will be taking Statin drugs. I know it has side effects, but that's better than small dense LDL. Based on Dr Davis's previous response, for apoE, sometimes we have to go to Statin for the rescue. (My doc was pushing statin really hard on me, and I have been resisting that for the last year)

    otter

  • Joyce

    9/19/2011 5:50:45 PM |

    Dr. Davis, you are so funny.  We'll take your book....typos and all!  Now...how about a cookbook to compliment Wheat Belly/  PLEASE????

  • nina

    9/19/2011 7:41:34 PM |

    Sorry I missed the link:

    http://suzanneloomscreativity.blogspot.com/2011/09/lowering-blood-sugar.html

    Nina

  • PeteKl

    9/19/2011 9:24:31 PM |

    Hi Kira,

    Just out of curiosity, could you summarize your "paleo style of eating".  I have a good friend of mine who has similar numbers (low trigs, high HDL, high LDL).  I would describe her diet as "low-carb (no sugar, no grains), low-veggie (under 15%), high meat, high sat-fat (particularly cheese, eggs and coconut)".  Is your diet somewhat similar?  I would be interested to know how the two of you compare.

  • Dr. William Davis

    9/20/2011 12:36:46 PM |

    NMR is my preferred method, since it yields the LDL particle number, what I believe should be the gold standard.

  • Dr. William Davis

    9/20/2011 12:38:12 PM |

    Thanks for asking, Joyce! I've had very preliminary conversations with my editor, but nothing firm yet.

    In the meantime, in addition to the discussion on this blog, see the Wheat Belly Blog, where I will publish recipes one by one.

  • Dr. William Davis

    9/20/2011 12:41:39 PM |

    Hi, Kira--

    You have a surprising dominance of small LDL particles, despite your slender build and lifestyle (LDL 3+4 divided by "real" LDL). This is likely genetically-determined. The means of correcting this is beyond the scope of this blog, unfortunately. You might consider joining the discussion in the Track Your Plaque website.

    The vitamin D issue is common, an impaired or lost ability to activate vit D in the skin. It means doing it orally.

  • Adam

    9/20/2011 6:40:19 PM |

    Dr. Davis. I'm a type 1 diabetic who is on a low carb diet (mostly primal-esque) with only meat and veg. No fruit, no grains, no legumes. I lost 14 kgs in the first three months, then stabalized at around 89 kgs. Granted my fat is going down a wee bit as muscle mass increases (doing the slow burn exercises, plus HIIT training and martial arts). That is the background.

    The reason I'm posting here is confusion about cholesterol. I just got my latest results back from the lab, and they are the same. While my HbA1C is 5.3 (not bad), my cholesterol numbers don't look hot. Tryglicerides are fine (as I've stopped losing weight quickly), but HDL is low at 39, and LDL (doctor forgot to put in particle size check, but it cna't be that good as I'm a diabetic) was 150 on the spot. This was measured, not calculated.

    I take ~7k miligrams (or whatever the measurement is) of fish oil a day. Well, 7k of EHA/DHA, more in total quanity including inert substances. With my exercise, low carb diet, and fish oil supplements, how is it that my HDL are still so low? Any advice?

    Thanks!

  • Dr. William Davis

    9/20/2011 11:08:46 PM |

    Hi, Adam--

    How timely! See the next post after the one you responded to in which I discuss the transient effects of weight loss, including drops in HDL that rebound over time.

    Also, have you address vitamin D normalization? I aim for 60-70 ng/ml, which usually requires around 6000 units per day (gelcaps or drops only); the HDL-raising effect develops over a year or longer.

  • Adam

    9/21/2011 1:01:18 PM |

    Dr Davis,

    A pleasure to make your (virtual) acquaintance! My vitamin D, according to my last test (results came in yesterday, as I mentioned) levels are 59. A wee bit low, but not too bad, I think.

    I've been consistently 88/89kg for three months (I've been low carb/primal for 6 months total), so haven't lost any weight in the past three months, but still my HDL levels are very low. Do you have any suggestions?

    Cheers,

    Adam

  • Adam

    9/21/2011 1:03:52 PM |

    P.S. I'm pretty sure I've stabalized, as my triglycerides were at 29 or 39 (can't remember off hand, but pretty low). But still I had the low HDL and high LDL?

  • Dr. William Davis

    9/21/2011 9:37:43 PM |

    Hi, Adam--

    Of course, you are wheat-free, low-carb in addition to your vitamin D? Omega-3 fatty acids?

    Note that doing the diet and taking the vitamin D yield rises over 1-2 years. Patience is required.

    Consider a little red wine and dark chocolate, as well.

  • Adam

    9/22/2011 5:10:38 AM |

    Thanks for the response! Yes, I am completely wheat free (and was before I read your book, which was excellent). I am very low carb due to the diabetes. My HDL did go from 29 to 39 this last test (after 6 months), so I suppose, as long as maintaining this diet will continue to increase my HDL, I am ok. My concern isn't immediate gratification but more continuous improvement.

    I'll come bug you again in 3 months if my HDL doesn't continue to increase Smile

    Many thanks!
    ---Adam

    P.S. I've never been accused of not drinking enough red wine Smile While I've been beer free for 6 or 7 months now, I do go through ~2 bottles of red a week.

  • Adam

    9/23/2011 1:35:08 PM |

    Hah! Me too, because if my HDL doesn't start going up I'm gonna freak as I don't know what else to about my numbers. Diet is about as stripped down as it can be, and I'm exercising as much as is reasonable.

    --Adam

  • Kira

    9/24/2011 6:23:22 AM |

    HI Peter. I would say  that my diet could pretty similar, with the exception that I am still eating some low-glycmic fruit everyday (some cantaloup, grapefruits, berries) and eat lots of veggies.

  • Kira

    9/24/2011 6:29:11 AM |

    Dr. Davis, thnx for your reply. I understand this is a blog and it is hard to go into details here, but would you say that it is worth for me to try change this situation by changing the die to using less saturated fat? and would NMR test clarify anything?

    PS How do I further discuss this issue "by joining the discussion in the Track Your Plaque website"?

    Thnx AGAINSmile

  • ShottleBop

    9/25/2011 3:47:09 PM |

    My numbers are like Bill's.  I was diagnosed as pre-diabetic in February, 2008 (today, I'd have been diagnosed as Type 2; my A1c was 6.5, and my FBGs were 127 and 123).  Started low-carbing shortly after that:  cut out grains, starchy veggies, almost all fruit, all milk (still use heavy cream and eat cheese).   My most recent blood lipids (accounting for some variation, but roughly consistent in pattern over the past three years):

    TC:  381
    LDL (direct):  279 (291 calculated)
    HDL:  80 (was 40 at diagnosis)
    Trigs:  52

    (At diagnosis, my numbers were:
    TC: 281
    LDL (direct) 215
    HDL: 40
    Trig: 142)

    I lost 65 pounds in the first 9 months after diagnosis, and, since then, have regained approximately 25 pounds (mostly muscle).  Weight has been stable for months.  My doctor is talking statins, again--which I plan to continue resisting.  I have ordered an NMR test, and will see what it has to say about my particle size.

  • Dr. William Davis

    9/26/2011 12:39:56 PM |

    Hi, Shottle--

    Good plan. I wouldn't be surprised if NMR sheds an entirely different light on your values.

  • ShottleBop

    9/29/2011 4:23:57 PM |

    They drew the blood this morning.

  • Bob

    9/30/2011 11:14:10 PM |

    Dr. Davis, I had my NMR test and the doctor who looked at it suggests that I have familial hypercholesterolemia. My LDL-P 3158
    LDL-C 280 HDL-C 58, TGL 105, HDL-P 28.0 small LDL-P 1122,
    LDL 21.7, LP-IR-33. I have been on no carb, no sugar, no wheat, or fruit for the last 14 months. Have been eating fatty meat twice a day and also eggs. Before I started eating beef, I was eating low carb, very little sat. fat. I was eating a lot of skinless chicken breast, and canned salmon, veggies, nuts, fruit but almost no beef. My LDL according to the basic lipid test was a little high but not crazy high. My HDL was in mid 30's. and trigs were high. I changed to a high saturated fat diet to raise HDL and lower trigs. I have been taking 1 gram of fish oil 2X daily. Is it possible that the fish oil is having an effect on my LDL? Not sure what to do about my diet. Obviously I won't go back to sugar and wheat but what about all the meat I have been eating. Would it be better to go back to skinless chicken and egg beaters even if it means my HDL going down? Just not sure what to do. Doctor believes I am at high risk since my father died at age 62 of sudden death.
    Thanks,
    Bob

  • Dr. William Davis

    10/1/2011 1:48:14 PM |

    Hi, Bob--

    This is a tough situation that, unfortunately, cannot be remedied diet alone. I hate saying that.

    Like people with apo E4, familial heterozygous hypercholesterolemia people are fat sensitive. First order of nutritional business remains carb-restriction to minimize small LDL particles, but you can still show large increases in large LDL with fat intake. If apo E4 is present, too, then even something as great as fish oil can increase LDL measures. However, the dose of fish oil you are using is very small and not a likely factor.

  • Bob

    10/1/2011 2:57:34 PM |

    Thanks for the reply Dr. Davis. I know I won't go back to carbs and sugar, but what about beef. I have eaten almost nothing but beef the last 14 months. Would I be better off going back to skinless chicken breast? Egg Beaters, instead of eggs? Olive oil instead of butter? I know in the past when I limited saturated fat my HDL dropped to mid 30's.
    Bob

  • Dr. William Davis

    10/2/2011 2:46:17 PM |

    Hi, Bob--

    I think we could make a strong argument in favor of variety in diet and that includes meat sources. Yes, I think a broader range of meats (if you eat them; I don't want to sound like a bloodthirsty carnivore; I don't even like meat, personally) is better--fish, shellfish, fowl, pork, as well as eggs.

  • ShottleBop

    10/3/2011 10:02:47 PM |

    Results came back today:
    TC:  373 mg/dL (ref <200)
    LDL-C:  282 mg/dL (ref = 40)
    Trigs:  47 mg/dL (ref < 150)
    Large VLDL:  <0.7 (ref <=2.7)
    LDL-P:  1793 nmol/L (ref = 30.5)
    Large HDL-P:  14.2 umol/L (ref >=4.8)
    Small LDL-P:  146 nmol/L (ref  20.5)
    HDL size:  10.0 nm (ref >=9.2)
    VLDL concentration was too low to determine a size
    According to the interpretive information:
    My HDL-P (total) of 39.1 places me in the lowest category of risk (it is beyone "high")
    My small LDL-P places me well below the 25th percentile (while slightly higher than the "low" level of 117), and is indicative of lower risk for CVD
    My LDL size places me well above the 75th percentile, and well into Pattern A territory (75th percentile level is 20.6), and is indicative of lower risk for CVD

  • ShottleBop

    10/3/2011 10:04:16 PM |

    Correction:  My LDL-C was 282, vs. a reference of " 40"

  • ShottleBop

    10/3/2011 10:06:37 PM |

    I give up.  I am typing things in correctly, and the comment system is dropping words (maybe it's interpreting my use of "greater than" and "less than" symbols as markup code?).  My HDL-C was 82.  The reference level is greater than 40.  My LDL-C was 282; the reference level is less than 100.

  • ShottleBop

    10/3/2011 10:09:37 PM |

    I see it dropped more information than I thought at first.  No matter, the conclusion stays the same: except for my LDL particle number and concentration, all of my lipid values indicate that I am at lower (or much lower) than average risk of CVD.  Now if only my body takes that to heart . . ..

  • ShottleBop

    10/3/2011 10:16:32 PM |

    LDL particle size was 22.1
    HDL-P was 39.1 umol/L

  • Dr. William Davis

    10/4/2011 2:41:25 AM |

    Hi, Shottle--

    Your values highlight this tremendous void we have in knowing just what to do about nearly "pure" large LDL particles.

    In other words, you have lots of LDL particles, but they are nearly all the more benign large variety. What level of large LDL particles are "allowable" before they contribute to atherosclerotic plaque formation? Not known. My preference would be, given the extreme abundance of large LDL, to reduce with statin drug. I hate to say this, but this is the occasional exception in which I believe that statins might indeed be beneficial. This is not to be confused with the general and absurd overuse of the drugs, but an application for a very specific genetic variant.

  • Louise

    12/5/2011 10:58:49 PM |

    At last I have had an NMR.  Thank you for the suggestion of PrivateMDlabs.com.  I can recommend this
    to others who find their doctor unwilling to order tests.
    I am pondering my results, trying to figure out if they are okay, or if I need to cut back on fat now, or go lower with carb reduction. What are your thoughts, Dr Davis?
       LDL Particle Number  1091  ( IS this too high??)
        Small LDL - P    129
          LDL size     21
        Large VLDL - P   < 0.7
           Large HDL - P        12.1
            HDL size           9.7
          LP - IR score    11
    Triglycerides are 32  ( lower since I"ve gone completely
    grain free since my last lipid panel)

  • Dr. William Davis

    12/6/2011 5:26:54 PM |

    These values are excellent, Louise! The only less than perfect value is the large HDL, but this tends to drift higher very slowly.

  • GoodStew

    5/11/2013 1:56:57 AM |

    Seems particle size doesn't matter as much as particle number. According to Dr. Peter Attia, a particle is a particle.  More than 1000 is a risk factor whether they're small, medium or large and fluffy.

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