When MIGHT statins be helpful?

7. April 2011 William Davis (17)
I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

5. April 2011 William Davis (0)
Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

4. April 2011 William Davis (5)
The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

3. April 2011 William Davis (13)
While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.

Wheat brain

30. March 2011 William Davis (52)
Among the most common effects of wheat are those on the brain.

Consume wheat and susceptible individuals will experience a subtle euphoria. Others experience mental cloudiness or sleepiness. (This is what I personally get.)

It gets worse. Children with ADHD and autism have difficulty concentrating on a task and have behavioral outbursts after a cookie. Schizophrenics experience paranoid delusions, auditory hallucinations, and worsening of social detachment. People with bipolar disorder can have the manic phase triggered by a breadcrumb. All these effects are blocked by administering drugs that block the brain's opiate receptors. (This is why, by the way, a drug company is planning to release an oral agent, naltrexone, formerly administered to heroin addicts to help control addiction, for weight loss: block the euphoric effect, take away the temptation, lose weight.)

Here is Heart Scan Blog reader, Nicole's, mental fog story:

I have been grain-free (no gluten free grains either) for quite a long time (about a year and a half). Earlier this week, I decided to try white bread and pasta. The experiment only lasted two days. I had horrible terminal insomnia both nights, causing me on the second night to wake up at 2:30 am unable to get back to sleep at all. I felt drugged and in a mind-fog all the next day and even dozed off a few times! Luckily I had the day off work.

I had very bad forgetfulness also. I forgot that I left my bag and groceries at work, so I had to go back for them. Then I had to use my husband's keys to get in because I thought my keys were in my bag, but it turns out they were in my pocket. Then I got my bag, set the alarm, locked the door and then realized I forgot my groceries. So I had to re-open the door, unset the alarm, and go back for the groceries. Then I locked the door, forgetting to set the alarm, so I had to unlock it, open up and set the alarm. It was just ridiculous, I am NEVER like that!

In addition to the insomnia and forgetfulness, I also had horrible anxiety and paranoia, almost to the point of panic. Which I NEVER have, I am usually very easy-going, even-tempered, and worry-free. But this was horrible, I really was quite paranoid and anxious about everything. Weird!

And the worst, was that in just two days of eating wheat, I gained 4 lbs and 2% bodyfat!! It's two days wheat-free now, and it's finally going back down, but wow. Just two days of wheat-eating caused that much weight and fat gain!

Anyway, I've learned my lesson and will continue to avoid grains (including gluten free grains) entirely.

Eat more "healthy whole grains"? Modern dwarf Triticum aestivum, perverted even further by agricultural geneticists and modern agribusiness, subsidized by the U.S. government to permit $5 pizza, is better than any terrorist plot to discombobulate the health and performance of the American people.

The Westman Diet

27. March 2011 William Davis (71)
Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek.

Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days).

Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables.

After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications.

That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal.

Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes.

This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.

These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics.

All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes.

(This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)

Handy dandy carb index

25. March 2011 William Davis (21)
There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences.

One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet.

Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test.

For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c.

HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.)

HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less.

HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)

HbA1c of diabetics: 6.5% or greater.

Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics.

With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar.

Battery acid and oatmeal

23. March 2011 William Davis (38)
Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."

Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus.

Know what food is the most potent source of sulfuric acid in the body? Oats.

Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.

Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic.

The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases.

Here's one reference for this effect.

What'll it be: Olive oil or bread?

21. March 2011 William Davis (0)
We frequently discuss the advisability of consuming fats, carbohydrates, and various types within each category.

But what's the worst of all? Combining fats with carbohydrates.

Putting aside the wheat-is-worst form of carbohydrate issue and treating bread as a prototypical carbohydrate, let's play out a typical scenario, a make-believe feeding study in which a theoretical person is fed specific foods.

John is our test person, a 40-year old, 5 ft 10 inch, 210 lb, BMI 27.7 (roughly the mean for the U.S.) He starts with an average American diet of approximately 55% carbohydrates and 30% fat. Starting lipoproteins (NMR):

LDL particle number 1800 nmol/L
Small LDL 923 nmol/L


(The LDL particle number of 1800 nmol/L translates to measured LDL cholesterol of 180 mg/dl, i.e., drop last digit or divide by 10.)

Also, calculated LDL cholesterol is 167 mg/dl (yes, underestimating "true" measured LDL), HDL 42 mg/dl, triglycerides 170 mg/dl.

We feed him a diet increased in carbohydrates and reduced in fat, especially saturated fat, with more breakfast cereals, breads and other wheat products, pasta, fruit juices and fruit, and potatoes. After four weeks:

LDL particle number 2200 nmol/L
Small LDL 1378 nmol/L

Note that LDL particle number has increased by 400 nmol/L due entirely to the increase in small LDL particles triggered by carbohydrate consumption. Lipids show calculated LDL cholesterol 159 mg/dl--yes, a decrease, HDL 40 mg/dl, triglycerides 189 mg/dl. (At this point, if John's primary care doctor saw these numbers, he would congratulate John on reducing his LDL cholesterol and/or suggest a fibrate drug to reduce triglycerides.)

John takes a rest for four weeks during which his lipoproteins revert back to their starting values. We then repeat the process, this time replacing most carbohydrate calories with fats, weighed heavily in favor of saturated fats like fatty red meats, butter and other full-fat dairy products. After four weeks:

LDL particle number 2400 nmol/L


Let's

Chocolate peanut butter cup smoothie

19. March 2011 William Davis (18)
Here's a simple recipe for chocolate peanut butter cup smoothie.

The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa.


Ingredients:
1/2 cup coconut milk
1 cup unsweetened almond milk
2 tablespoons cocoa powder (without alkali)
2 tablespoons shredded coconut (unsweetened)
1 tablespoon ground flaxseed
1 teaspoon almond extract
1 1/2 tablespoons natural peanut, almond, or sunflower seed butter
Non-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)
4 ice cubes

Combine ingredients in blender. Blend and serve.

If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand.

For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener.

The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe.
I Wish I Had Lipoprotein(a)!

I Wish I Had Lipoprotein(a)!

8. August 2012 William Davis (33)
Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.


In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.
Tags :

Comments (33) -

  • Bill Davis

    8/8/2012 1:17:58 PM |

    I have Lp(a) and am working on reducing it.
    Have been off wheat for several years now and on a low-carb diet. Hope I find that diet as well as fish oil, thyroid treatment, niacin and DHEA will bring it down.
    Thanks for making me feel special with this article! I have cross posted it. Scan coming up next month to give me a look at how I'm doing.
    The other Bill Davis

  • Joe

    8/8/2012 5:05:52 PM |

    I know this is probably a stupid question: but who doesn't have Lp(a)? My last VAP said that I have a Lp(a) of 7.0 and that <10.0 is preferred. Do some people actually have zero Lp(a)?

    Thanks!

  • randallbb

    8/9/2012 3:01:37 PM |

    I too am high Lp(a) and fit largely the profile Dr. Davis has outlined.  Am working on the Lp(a) with all guns blazing!  My new TYP lifestyle along with high amounts of fish oil and Niacin have brought it down markedly in just six months (from 61mg to 46mg on the NMR profile).  Am eating lots of cheese, nuts, etc, so am glad to hear that fats are a good thing!  Dr. Davis' post here reminds me to keep limited my carb intake!

  • Holly

    8/9/2012 10:44:08 PM |

    Any ideas why these traits would correlate with Lp(a)?

  • aerobic1

    8/11/2012 2:28:01 PM |

    Joe:

    Yes, some people do have "zero" Lp(a).  It is partly determined by your genetics which you have no control over.  But, as Dr. Davis suggests you gain gain control over your Lp(a) with dietary interventions such as elimination of wheat and other refined carbs, along with taking a few targeted supplements.  His interventions do not involve pharmaceutical drugs as there are no drugs that effectively treat Lp(a).

    Three years ago my first VAP test revealed a Lp(a) level of 22.  Three years of following Dr. Davi's advice my level is now 3.  For more information go to http://www.trackyourplaque.com/default.aspx.

  • Joe

    8/11/2012 4:59:41 PM |

    Thanks for the feedback!
    On the other hand, aren't you on the way to having no Lp(a)?  From 22 to 3?
    I'm still not sure why having "high" Lp(a) is a good thing. I'm still confused. Frown

  • jpatti

    8/11/2012 9:08:51 PM |

    We're also good-looking.  And very sexy.  And surprisingly modest!  ;)

    So why the heck would the thirst thing be going on?  I don't get it.  

    I have this issue; I have to carry drinks all the time or I completely forget about drinking.  I never go anywhere without carrying drinks cause I don't remember until I've got a killer headache.  I've got a giant mug of coffee and a liter of ice water flavored with lime shrub sitting next to me right now.  

    It's not that I'm not thirsty, if you ask me, I become aware of thirst.  It's just that "thirsty" is not something I am aware of at all.  I don't notice it unless I ASK myself if I'm thirsty.  

    I'm also ridiculously picky, I can have a drink sitting next to me, but if the ice has melted, I don't "want" it no matter how thirsty I am.  

    I don't understand why I'm like this.

  • aerobic1

    8/12/2012 2:48:06 AM |

    Joe:  
    There is nothing good whatsoever about having any measurable level of Lp(a).  Zero Lp(a) level should be your goal.  The personality characteristics Dr. Davis pointed out are just some typical observations of Lp(a)er's but do not assume the higher your Lp(a) is that the more intelligent, better at math or athletics, etc. you will become.  Lp(a) offers no advantage in that regard.

    There is plenty of good reading and advice from Dr. Davis on this subject on this blog on what Lp(a) is and how to self-manage it.  http://blog.trackyourplaque.com/category/lipoproteina.  Most all doctors are not well informed on this subject and therefore do not know how to treat it.

  • aerobic1

    8/12/2012 4:52:33 AM |

    jpatti:

    The sensation of thirst is governed by the Hypothalamus and Limbic System of the brain.  I do not have an understanding of why people with Lp(a) demonstrate this unusual thirst pattern that Dr. Davis has observed in people with Lp(a).  Here is a good explanation of how the typical thirst mechanism works.  http://www.enotes.com/thirst-reference/thirst.  

    Perhaps the normal brain hormone driven thirst mechanism in people with Lp(a) "malfunctions" and may not be producing enough arginine vasopressin to enhance thirst.  The relationship of renin, angiotensin II, and aldosterone also control water retension and thirst and may play a role too.

  • Joe

    8/12/2012 6:36:30 PM |

    Aerobic:
    Thanks again. I followed that link and it reiterated Dr. Davis' protocol, of: " i.e., wheat elimination followed by elimination of cornstarch, oats, and sugars; high-dose fish oil (total daily EPA + DHA of 6000 mg/day); vitamin D supplementation sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml; iodine supplementation; and thyroid normalization which, in Ted’s case, required supplementation with the T3 thyroid hormone, liothyronine, at a small dose. "

    And I follow that protocol pretty closely (I don't take quite that much fish-oil).  My thyroid is fine. I have Pattern "A" LDL. Vitamin D of 90ng/ml. My TC is "high" but I have great trig and HDL numbers and ratios. My Lp(a) again is 7, which is well under the "reference range" of  <10 (according to VAP). But I'm unable to find anything anywhere that explains why having a zero Lp(a) is best, or what the mechanism is that makes it best. I'll keep looking around. Thanks for the help!

  • Joanna

    8/13/2012 8:16:28 PM |

    So we requested our doctor order an Lp(a) test along with several other blood tests that were being done - and later find out that our insurance company (Humana) will not cover the cost of the test, they gave some reason like it wasn't scientifically proven to be useful!!!  It's $65 so not sure if it would be worth fighting them on this one since they have been pretty good about covering most things.

  • Mark

    8/14/2012 2:59:56 AM |

    Hi Dr. Davis,
    I’m 47 yrs old. I’ve had migraines since I was a teen and I developed Athsma this past January (hate it). During the process of discovery the drs found I have a 50% blockage in one of the 5, non critical, arteries running along the back of my heart. Scared me, to say the least. I’ve always eaten quite healthfully (for what I knew), am thin @ 6′ 1″/155lbs (was 175lbs in Jan.). Had:
    Total Cholesterol of 200
    LDL of 146
    HDL of 50

    Drs wanted me to do Lipitor. Researched and said, “No, thanks.” Started exercising 5-6 days/wk (lifting + walk/run), taking red yeast rice, fish oils, fish, no meat, no dairy, no eggs, lots of veggies/fruit, etc., but still eat beans, oats (every AM), occasional wraps. After 6 wks my blood work (VAP) was as follows:
    LDL=86
    HDL=43
    VLDL=17
    TOT. CHOL=146
    Trigycerides=66
    Non-HDL (LDL+VLDL)=103.

    Seemed GREAT to me! The dr wasn’t impressed. Said my ‘particle size’ was small: LDL1(a)=8.1, LDL2(a)=0, LDL3(b)=39.5, LDL4(b)=24.9. Density Pattern=B.

    I’ve continued but don’t know how to elevate my HDL and reduce the particle size/change the pattern to the more favorable ‘A’. Getting down about this. Working hard but, seems like I can’t find answers that work, anywhere! What might you would work in my situation? Also, Is niacin ANDRed Yeast Rice a bad idea?
    I’ll hang up and listen. Thank you,
    Mark

  • Will

    8/14/2012 3:03:09 PM |

    Dr. Davis,

    Do you have any comments or response to the study released yesterday at the University of Western Ontario, comparing the risk of regular consumption of egg yolks to smoking on the increase of arterial plaque?

  • JoAnne

    8/15/2012 1:08:25 AM |

    Dr Davis, I recently had had a NMR LipoProfile done, but I don’t understand the numbers. I think it’s saying my LDL particle size is pattern A (good), but the total LDL-P number of 1985 nmoI/L is bad. And the HDL at 79 mg is good, but the TC at 307 is bad…. I’m so confused. Can you please summarize? I’ve been looking at the TYP website and I’m ready to join.

    LDL-P    1985 nmoI/L  (LDL Particle number)

    LDL-C    212 mg/dL  (calculated)
    HDL-C  79 mg/dL
    Triglycerides  82 mg/dL
    Total Cholesterol  307 mg/dL

    LDL & HDL Particles
    HDL-P   40.8 μmoI/L  (total)
    Small LDL-P  106 nmoI/L
    LDL size  22.1 nm

    Lipoprotein markers assoc with insulin resistance & diabetes risk
    Large VLDL-P  0.7 nmoI/L
    Small LDL-P    106 nmoI/L
    Large HDL-P  15.8 μmoI/L
    VLDL size    32.9 nm
    LDL size    22.1 nm
    HDL size    9.9 nm

    Insulin resistance score  0-100
    LP-IR score    5

  • kimsuoil

    8/15/2012 2:15:14 AM |

    Dr. Davis, I have Lp(a) and all of the traits above. Don't really know my IQ, but I am a Petroleum Geologist, been a runner for over 32 years,  can go many hours without water (ran a marathon in 3 hrs and 3 minutes when I was 24 in New Orleans and only had a small cup of water at the halfway point).  I have no problem eliminating foods and have high willpower to food.

    Before joining your Track Your Plaque program 3 years ago, I was on the "low fat"  high carb Am. Heart Assoc. recommended diet for many years.  At 48 I discovered that I had massive heart disease and received 6 stents.
    I now have to limit my carbs to very low to keep my small LDL particles somewhat low.

    Good news is now at 53 years old my carotids are getting better flow since on the TYP diet when I got my last carotid echo.

  • Gene K

    8/15/2012 5:59:29 PM |

    @Joanna
    We have coverage thru Blue Cross Blue Shield, and they require extensive review of why I would need an NMR or an Lp(a) test, after which they will decide whether to cover or not. I decided it was too much of a pain, so I order these tests thru privatemdlabs, and use their receipt to get reimbursed from my flexible spending account. If you have an FSA, you could do that, too.

  • Joanna

    8/15/2012 8:18:23 PM |

    Nope, no FSA account so that's not an option and they already have extensive records of why it would be warranted (if they even looked at medical expenses for the past year it would be obvious!)  Thanks for the tip though.

  • Dr. Davis

    8/17/2012 2:36:21 AM |

    Hey, Kim!

    Yes, we have to reverse this incredibly stupid tidal wave of low-fat that is enormously destructive.

    The proof is in the (carotid) pudding!

  • Dr. Davis

    8/17/2012 2:40:41 AM |

    There are a number of possibilities to explain this pattern, JoAnne.

    Among them:

    --Hypothyroidism
    --Apo E4 genetic type
    --Other genetic patterns

    Unfortunately, this is a pattern that may be difficult to correct with diet. You might also consider an HDL Labs sterol absorption panel to decide what role diet plays.

  • Dr. Davis

    8/17/2012 2:43:50 AM |

    This is a pattern that is highly responsive to diet, such as the diet used in the Track Your Plaque program, the diet discussed in these pages, and the diet I articulate in my book, Wheat Belly.

    By the way, you are currently on a diet that makes this pattern worse. Your diet of avoiding meats and eggs with lots of fruits causes the small LDL pattern and heart disease. And it sounds like you have an intellectually challenged doctor who wants to prescribe drugs but doesn't understand that your diet is contributing or outright causing your pattern.

  • Dr. Davis

    8/17/2012 2:45:54 AM |

    Nobody does.

    It is likely that the gene for the apo(a) protein of Lp(a) is somehow linked to a gene for thirst triggering and nothing more.

    More of a curiosity than anything else.

  • steve

    8/19/2012 1:36:11 AM |

    Hi Dr. Davis:
    Can LDL-P level ever be to low? I have heard lower is better, but when you get below 500, most of that can be small LDL-P.
    Thanks

  • Dr. Davis

    8/23/2012 2:00:59 PM |

    Yes, it can.

    But it should be mostly, if not all, large particles if you are following the diet advised here.

  • steve

    8/26/2012 8:39:17 PM |

    i do follow the diet, but unfortunately generate much in the way of small LDL-P
    I eat no wheat, small amounts of rice and potatoes, no other grains or sugars.  TRGS  were 26 which i thought  is an indication of carb intake.  Am guessing it is just genetics.
    How low is low for LDL-P and do you have any studies you can point that indite small particles?  All research I have seen indite LDL-P and say size does not matter.  Would be interested in seeing studies that show otherwise
    Thanks

  • jpatti

    8/28/2012 7:46:26 PM |

    Yes, I knew the hypothalamus was involved with thirst and the adrenals involved with electrolyte balance.

    Except... just last week, I had a board-certified endocrinologist tell me that ONLY the heart, liver and kidneys are involved in fluid/electrolyte balance:  
    http://gapsfort2.blogspot.com/2012/08/i-am-just-so-freaking-angry.html

  • Susan

    10/4/2012 9:59:33 PM |

    My pattern is very similar and I have had the sterol absorption panel, though I don't know what it means. Campesterol is optimal at 2.22, Campesterol ratio is Hypo at 63, Sitosterol is Hyper at 3.23, Sitosterol ratio is optimal at 88, Cholestanol is Hyper at 5.89 and Cholestanol ratio is Optimal at 172. What does this tell us?

  • Kindred

    10/31/2012 4:53:42 PM |

    My LP(a) was 167.  I got it down, in three months, to 22 using the strict vegan, Forks Over Knives approach coupled with 1500 mg of niacin before going to bed.  My math skills are deplorable as I have severe discalculia (the math version of dyslexia which I also have.)  I'm not competitive at all so, although very coordinated and active, I'm not athletic.  I drink lemon water or dandelion/chicory coffee frequently and frequently get up in the middle of the night for a glass of lemon water. I'm not diabetic and am tested for this annually.   I graze between  meals on celery sticks.   Also, I'm 1/8 Native American Indian. We are suppose to have low levels of LP(a.)

    I lightened up on the vegan diet using olive oil for cooking and my LP(a) rose in 3 months to 67 so it's back to Forks Over Knives again.

  • darin

    12/29/2012 5:47:33 PM |

    Confused, would this be the same thing as Lp(a) mass (mg/dl) i had on a recent Health diagnostics test?
    Mine is showing 44 and its supposed to be less than 30.

    There was also a Lp (a) cholesterol (mg/dl) and mine was 8- supposed to be <3

    Thanks

  • Fred Rutherford

    6/17/2013 5:00:36 AM |

    I have a lipid disorder. My doctor checks lpa once a month. Says thou I have minimal body fat I have to take cholesterol meds. Because my lpa is 14 times higher than what is considered high risk. This putting me at risk of blood clots. I under go quarterly ulta sounds of vascular system as well as annual Hart caths. A high price for being smarter than the average bear. Don't ya think?

  • Dr. Davis

    6/18/2013 1:29:29 AM |

    No, you have been misled.

    What you need are new doctors, plain and simple.

  • Mathieu Gagné

    6/18/2013 5:17:58 PM |

    That is very interesting! I never heard of this before, but it seems to fit to me pretty well. I have high IQ, I'm a physicist, don't drink enough water and would be fairly athletic if it wasn't for my crohn disease. The impact of giving up grains was huge on my health! A quick search and I've found this link between high Lipoprotein(a) and crohn disease:
    http://www.ncbi.nlm.nih.gov/pubmed/11742189

    It would be interesting to ask my doctor about it!

  • Mary Ann Joyce

    2/15/2014 8:07:55 PM |

    I've the Berkley tests three or four times, and my Lp(a) was 217 in 2007; the latest test shows 80Lp(a).
    I have been on Crestor for a very long time, and now realize it does noting to lower the Lp(a).  On the latest test, my small particle was 21.2 and the large was 11.4.  What does this mean?
    I want to get off the Crestor and onto the niacin, etc., including pomegranate juice which, I understand, has properties that will lower the Lp(a).  I am aiming to cut carbohydrates out completely as well as reduce sugar to near zero.  Do any of you have suggestions for me?  Even though I am 70 years old, I am not ready for a stroke nor MI.  Thanks!

  • Sandra Tremulis- Founder Lipoprotein(a) Foundation

    5/7/2014 6:12:44 PM |

    For those of you interested there is now a foundation for high Lipoprotein(a)  www.lipoproteinafoundation.org

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The battle for natural hormones

18. April 2007 William Davis (0)
The battle for preservation of availability of compounded natural hormones goes on.

It started with pharmaceutical manufacturer, Wyeth, who petitioned the FDA to disallow the mixing of pharmaceuticals, especially natural human hormones, by specially trained pharmacists at what are called "compounding pharmacies." These are pharmacies that have special equipment and where trained pharmacists can mix up specific preparations for dispensing. These are available by prescription.

For instance, I have been prescribing natural human testosterone and progesterone for nearly 10 years. I have found service to be excellent, with lots of learning materials provided to patients by the pharmacy. The pharmacists I've spoken to have been courteous and knowledgeable. Compounded hormones are also shockingly less expensive. While a testosterone patch from a pharmaceutical company costs around $4.00 per day, the same quantity of testosterone cream formulated by a compouding pharmacy costs around $0.50 per day--87.5% less.

Wyeth hides behind a smoke screen of concern over quality. But the price differences tells the entire story: they want to eliminate the inexpensive competition and hold us all hostage to the far more expensive, often inferior products that they produce. They'd sooner force a woman to use horse-derived Premarin than to allow her access to human estrogens and progesterone.

To me, this is an outrageous affront to our freedom of choice, both as consumers as well as a physician. If you feel as strongly as I do about opposing the unfair and bullying ways of Wyeth Pharmaceuticals and the FDA, the P2C2 association of compounding pharmacists makes writing a letter to your Senator easy by going to

http://iacprx.convio.net/site/PageServer?pagename=P2C2

Just enter your info and personalize the comments, and the e-mails will be generated for you.

Lipitor and memory

17. April 2007 William Davis (2)
At first, I was skeptical. A book from a nutty author and physician named Duane Graveline kept on coming up in conversations with patients. His book, Lipitor: Thief of Memory , details his personal experience with dramatic changes in memory and thought while taking Lipitor.



Now this is a drug that I've seen used thousands of times. But I've now seen about a dozen people who have had distinct struggles with memory and clarity of thinking while taking Lipitor. Most took doses of 40 mg per day or more, though an occasional person takes as little as 10 mg. The association seems to be undeniable, since it improves after two weeks off the drug, recurs when resumed. Just today, I saw two people where this effect may be an issue.

Curiously, I've not seen it with any other statin agent. Unfortunately, uncovering any scientific data on the issue is a hopeless quest. Either it's very uncommon or, worse, the data has been suppressed.

Any way, I believe that Dr. Graveline was right: Lipitor, in a small number of people, does indeed seem to exert real detrimental effects on the mind.

If you take Lipitor, should you stop it in fear of long-term effects on your mental capacity? I think it's premature to toss the drug out based on this relatively uncommon relationship. This particular effect is likely to be idiosyncratic, i.e., peculiar to an occasional person but does not seem to apply to the majority, probably by some quirk of metabolism or penetrability of the barrier between the blood and nervous system tissue.

If, however, you feel that your thinking and memory have deteriorated on the drug, please speak to your doctor.

EKG's and heart disease

16. April 2007 William Davis (6)

How helpful are EKG's for detecting hidden heart disease?

I pose this question because several patients asked this question just this week. It's also a frequent point of confusion and misperception.

Your EKG is nothing more than an expression of the surface electrical activity emitted by heart muscle activity. Multiple (12) leads are attached to the body simply to provide various "views" of this electical activity. EKG, or sometimes "ECG", is short for "electrocardiogram".

What modifies this surface electrical activity? Anything that modifies the electrical activity within the heart itself, or interferes with the detection of the activity. An old heart attack modifies the patterns of electrical conduction in the heart and that can change your EKG. An ongoing heart heart attack likewise. High blood pressure commonly creates changes in the EKG, as does lung disease. A bellyache can change your EKG, as can a stroke. (These non-heart-related phenomena probably are often due to changes in autonomic, or "automatic," nervous system activity.) The heart generates electrical activity in a predictable sequence that generates the heart beat, or "rhythm". EKG's are useful for monitoring heart rhythm, also.

Does having plaque in your coronary arteries have any effect on the EKG? None whatsoever, unless plaque rupture caused heart attack or is about to cause heart attack. So, you can have a horrendous CT heart scan score of, say, 3000, yet maintain a perfectly normal EKG, as long as the heart muscle is normal.

Then why bother with these iffy tests? They are indeed useful to diagnose the cause of active symptoms. For instance, go to the ER with chest pain and an EKG could show changes suggesting that the chest pain is a heart attack. EKG's are also useful for future comparison. Any change in EKG can suggest certain things, like new heart rhythm disturbances unrelated to coronary plaque.

Think of your EKG as just like buying a used car. Say I'm trying to sell you my 1999 Buick Century. It looks pretty good from the outside and I tell you that it has 70,000 miles and runs well. You ask to open the hood, look in the interior and take it out for a drive. I tell you no, you can't do that.

Would you buy the car? Of course you wouldn't. You were permitted only a very superficial examination of the car. You have no idea what's going on inside. Just because the paint job looks brand new doesn't mean the engine and transmission are good.

The same with your EKG: It's a superficial look at one aspect of this used car called your heart. If the EKG is normal, that's good, just like a good exterior on the Buick. But you cannot assume that the heart is otherwise normal.

View the EKG as a simple, superficial test that can only provide minimal reassurance, no matter how often you have it done.

A new Track Your Plaque record

14. April 2007 William Davis (0)
Neal, a 40-year old school principal, and his young wife were terrified on learning of his CT heart scan score of 339, a concerningly high score for any age, particularly age 40.

To make matters worse, all of Neal's plaque was located in the critical left mainstem coronary artery, the shared stem of two of the three coronary arteries. A heart attack in this location is instantly fatal.

So, it was especially gratifying that Neal has set the Track Your Plaque record for largest magnitude of plaque reversal: 51% in his first year.

Studies that show a reduction in heart attack make the news. They talk about 1, 2, up to 6% regression, all achieved with high doses of statin drugs. Yet we are seeing huge, extraordinary quantities of heart disease reversal that haven't yet made headlines, amounts that far exceed those featured in the news. We should be encouraged by experiences like Neal's.

Watch for the upcoming Track Your Plaque newsletter for more details on Neal's story--how he came to the program, how he accomplished this huge effect, and why his experience was such a success. If you haven't yet subscribed, go to the www.cureality.com homepage and click on the upper right hand corner.

The Plavix Scam

12. April 2007 William Davis (3)
Periodically, I'll see a flurry of TV ads for Plavix. It comes with a polished computer-animated cartoon that shows how platelets clump and form a blood clot, causing heart attack.

Imagine there's a pile of oil-soaked rags in a corner of your garage. I come by and tell you to get a good fire extinguisher to keep next to the rag pile in case they spontaneously ignite.

Does that make sense to you?

Wouldn't it be better to get rid of the oily rags and forget about the fire extinguisher?

Plavix is the fire extinguisher. The oil rags are your coronary plaque. The solution is to gain control over plaque behavior. Unfortunately, the TV ads (intentionally, I suspect) give the impression that blood clots just form out of the blue for no reason. Of course that's not true. It requires active, growing, inflamed atheroslcerotic plaque that ruptures, uncovering the "angry" and platelet-adhering material underneath the thin covering or endothelial lining.

Urging everybody to take Plavix is absurd. The TV ads urge many people who have no business taking the drug to take it. There are, without a doubt, groups of people who are better off taking Plavix and aspirin: people who are in the midst of heart attack, people who have unstable plaque, people with recent stents or bypass. Perhaps people at high risk for plaque rupture, e.g., extensive coronary plaque that has continued to grow.

These tactics are consistent with the experiences I've had with the sales representatives from the company (when I used to actually talk to sales reps; my office is now barred from them). The reps very aggressively would urge me to consider having everyone take Plavix. No kidding.


For us, i.e., for people who just have a heart scan score but interested in engaging in a powerful program of prevention and reversal, Plavix rarely provides any advantage. The answer is, just like our oily rag analogy, control the plaque, not put out the fire.

Lipoprotein(a) and small LDL

11. April 2007 William Davis (0)
You won't find a lot of scientific validation for this, but it is my firm impression that small LDL, by some crazy means, has the capacity to "turn on" or "turn off" lipoprotein(a), Lp(a).

Recall that Lp(a) is a specific genetic trait, passed to us (if you have it) by mother or father. It falsely elevates LDL cholesterol and escalates heart disease risk more than just about any other known abnormality.

A frequent hint that Lp(a) might be present is a comment I hear often from patients: "My doctor said statin cholesterol drugs don't work for me. I tried them all and my cholesterol won't go down." Or, the result was substantially less than expected. That's because, when Lp(a) is lurking in your cholesterol value, it is unaffected by the statins.

It's been my in-the-trenches observation that, the more fully expressed the small LDL pattern becomes, the worse the Lp(a) behaves. In other words, if small LDL is suppressed effectively, Lp(a) doesn't seem to carry the same dangers as in someone who has plenty of small LDL. I don't know why this is. (I expect that the answer will come from someone like Dr. Marcovina at Stanford, who is at the forefront of Lp(a) structural research. Lp(a) is a complex molecule with several components. How and why it interacts with other particles remains a mystery.)

There are a little bit of data to confirm this. The Quebec Cardiovascular Study has presented some data to this effect, that the combination of small LDL particles and Lp(a) are a particularly lethal combination. We are trying to correlate our data from a CT heart score perspective to discern any statistical relationships.

This raises a very important therapeutic issue if you have Lp(a): the worst thing you can do if you have Lp(a) is become overweight. Excess abdominal fat is a huge trigger to create small LDL particles. Even though being overweight itself has no effect on the measured level of Lp(a), it activates small LDL which, in turn, throws gasoline on the Lp(a) fire.

If you have Lp(a), stay skinny.

Optimal medical therapy

9. April 2007 William Davis (6)
I was re-reading some of the details behind the recently announced COURAGE Trial comparing angioplasty/stent in 1100 people compared to "optimal" medical therapy in another 1100. You'll recall that no difference was found.

In particular, over approximately 5 years, 20% of participants in each group died, experienced heart attacks, or strokes. Of those treated with "timal" medical therapy, 32% ended up getting a procedure like stents or bypass anyway due to deteriorating symptoms.

What is "optimal" medical therapy? I bring this up again because the study investigators in COURAGE, as well as in similar trials, say this with a straight face. Optimal medical therapy means aspirin and/or Plavix (the anti-platelet, aspirin-like blood thinner); "aggressive" statin drug therapy to reduce LDL cholesterol to 60-85 mg/dl; and "anti-ischemic" therapy (that reduces angina and the phenomena of poor coronary blood flow) using nitroglycerin preparations, beta blockers, and other drugs.

I do give credit to the investigators for having the courage to perform this trial in a world hell bent on doing procedures and still reporting the neutral outcome. But the notion of "optimal" medical therapy begs for comment.

Indeed, this is regarded as optimal by most practitioners. Some would even argue excessive, based on the low LDL target achieved. Would you be satisfied with a 20% likelihood of heart attack, stroke, or death or 5 years, a 1 in 5 roll of the dice? I would not. Recall that we aim for near-total elimination of risk.

What could have been further "optimized"? Plenty. For instance:

--What is the real LDL, not the fabricated, calculated LDL? The two can be commonly 100 mg/dl different.

--How about raising HDL to 60 mgd/?

--What about reducing the proportion of small LDL particles? After all, small LDL is the number one cause of heart disease in the U.S., not high LDL.

--What is Lp(a)? If you treat LDL with a statin drug, Lp(a) is unaffected and continues to trigger huge plaque growth. You will fail if this is not identified and corrected.

--What is vitamin D3? One of the most powerful facilitators of plaque reversal I know of.

--What are triglycerides? Triglycerides create hidden particles in the blood like intermediate-density lipoprotein, potent triggers for coronary plaque growth. Speaking of intermediate-density lipoprotein, that's another very important pattern to identify, the after-eating persistence of dietary fats.

--Why aren't they taking fish oil? With a 28% reduction in heart attack and 45% reduction in sudden death from heart attack, this alone would have halved the number of "events" in the "optimal" medical treatment group.

Of course, there's more. But the idea that aspirin, statins, and anti-ischemic therapy is somehow optimal is silly and sad at the same time. But that's the bias. The COURAGE Trial does represent a step forward, a step away from the "stent everyone and everything" mentality that motivates my colleagues, aided and abetted by their co-conspirators, the hospitals. But you and I know better. "Optimal" medical therapy, in truth, can mean a far better approach that can dramatically reduce, perhaps eliminate, risks for events like heart attack. The conventional "optimal" medical therapy will suffice only if you're content with a 20% likelihood of heart attack, death or stroke, or a 32% likelihood of an urgent procedure in your future.

Niacin, postprandial patterns

9. April 2007 William Davis (0)
For a detailed report on the very important postprandial (after eating) patterns that contribute hugely to heart disease risk, read my recent article in Life Extension Magazine, available (no cost) at:

Uncovering a Hidden Source of Cardiovascular Disease Risk
at http://www.lef.org/magazine/mag2007/mar2007_report_heart_01.htm


For a report on using niacin to reduce risk of heart disease, see another report in the same issue of Life Extension:

Ask the Doctor: Using Niacin to Improve Cardiovascular Health
at
http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm.

Also, keep your eyes open for a lengthy report focused exclusively on the Track Your Plaque program in an upcoming issue of Life Extension. I'll provide links in this Blog when it comes out.

What's better than fish oil?

9. April 2007 William Davis (1)
One of the recent questions on our Track Your Plaque Forum related to what to do about a triglyceride level of 101 mg/dl while on fish oil.

Recall that, contary to conventional thinking like that articulated in the ATP-III cholesterol treatment guidelines, we aim to reduce triglycerides to 60 mg/dl or less. This is important to suppress the formation of abnormal triglyceride-containing lipoprotein particles, especially small LDL, reduced HDL, lack of healthy large HDL, VLDL. ATP-III advises a level of 150 mg/dl or less. Unfortunately, triglyceride levels this high guarantee appearance of all these undesirable particles and an increasing heart scan score.

What's better than 4000 mg of fish oil for its 1200 mg of EPA and DHA (omega-3 fatty acids)? More fish oil. In other words, the 4000 mg fish oil providing 1200 mg EPA + DHA is our minimum. A simple increase to 6000 mg to provide 1800 mg EPA + DHA is usually all that is necessary to reduce triglycerides and put a halt to the cascade of abnormal lipoprotein particles that trigger plaque growth. Occasionally, a somewhat higher dose may be required. Doses are best divided into two, with meals (e.g., three capsules twice a day).

Another important issue: An over-reliance on wheat products can also increase triglycerides. This includes any flour product like breads (regardless of whether it's white, whole wheat, or whole grain--they all raise triglycerides), pretzels, bagels, breakfast cereals, and pasta. A dramatic reduction in wheat-containing products will reduce triglycerides substantially, help you reduce your abdominal fat, reduce blood pressure, raise HDL and reduce small LDL, clear your mind, provide more energy, avoid afternoon "fogginess" . . . Huge benefits.

Valve disease and vitamin D

8. April 2007 William Davis (1)
There are two common forms of heart valve disease: aortic valve stenosis (stiffness) and insufficiency (leakiness), and mitral anular calcification.

Both valve issues are regarded as evidence of senescence, or aging--the older you are, the more likely you will have one or both. Both conditions involve progressive calcium deposition and, to some degree, cholesterol deposition. They might be regarded as phenomena of "wear and tear" just like hip arthritis.

There are no known therapies to stall or stop the development of mitral anular calcification. However, several attempts have been made over the years to identify treatments that can slow or stop the progression of aortic valve disease, which is becoming increasingly common and is addressed by surgical valve replacement when severe. The most recent trials have examined whether high-dose Lipitor (80 mg) has any effect (it did not) and high dose Crestor (40 mg), which slowed but did not stop the deterioration of stiff valves.

It's been my suspicion that vitamins D and K2 may play a crucial factor in valve health. After all, vitamin D is the master controller of calcium deposition. Preliminary data also suggest that people who are intentionally made vitamin K deficient with the drug, Coumadin, develop twice the calcium deposition on aortic valves that non-Coumadin takers develop.

I saw a patient Friday, Marianne. In addition to a moderate heart scan score of 379 at age 71, Marianne had a leaky (insufficient) aortic valve. By an echocardiogram 18 months ago, the valve was moderately leaky. I put Marianne on vitamin D, 4000 units, to raise her blood level to 50 ng/ml.

Last week, I asked Marianne to have another echocardiogram. This time, no leakiness whatsoever--none. I have never seen this happen before. Although Marianne is only one example and we don't want to extrapolate too far from the experience of one person, it's hard not to attribute this phenomenal response to vitamin D supplementation.

I wonder what would have happened if we had added vitamin K2, as well?

Anyway, just another potential wonderful effect of vitamin D restoration.