No more Lovaza

That's it: I will NEVER ever write another prescription for Lovaza.

I actually very rarely write a prescription for Lovaza, i.e., prescription fish oil. But this was the last straw.

I advised a patient that we've had good success using high-doses of fish oil to reduce lipoprotein(a), Lp(a). 6000 mg per day of the omega-3 component (EPA + DHA) from fish oil reduces Lp(a) in 60% of people after one year. (Recall that Lp(a) is the most aggressive known lipid-related cause of heart disease.)

The two preparations I generally suggest are either the very affordable Sam's Club Members Mark Triple-Strength Fish Oil with 900 mg EPA + DHA per capsule: 7 capsules per day. Another great product (my personal favorite because of its extreme purity--it doesn't even smell like fish oil): Pharmax Finest Pure Fish Oil with 1800 mg EPA + DHA per teaspoon: 3 to 3 1/2 teaspoons per day.

Both preparations work great and are quite affordable, given the high dose. For the Sam's Club preparation, it will cost around $30 per month, while the Pharmax liquid will run around $49 per month.

Well, the woman's husband insisted on a prescription for Lovaza. One Lovaza capsule contains 784 mg EPA + DHA per capsule: 7 to 8 capsules per day.

Here are some prices for Lovaza from online pharmacy discounters:
Prescription Giant: $78.99 for 30 capsules ($2.63 per capsule)
Planet Drugs Direct: $135 for 100 capsules ($1.35 per capsule)

These are lower than the prices I obtained in past by calling local pharmacies in my area, quite a bit lower, in fact.

Filling the Lovaza prescription at Prescription Giant will therefore cost $552.93 to $631.92 per month; at Planet Drugs Direct it will cost $283.50 to $324.00 per month. At local pharmacies, a similar 7 to 9 capsules Lovaza per day will cost upwards of $800 to $900 per month.

The patient's husband insisted on the Lovaza prescription because he knew that his insurance would cover it. When I pointed out that this was a large cost that would have to be borne by others in their healthcare premiums, he said that didn't matter to him.

I hesitated, but ended up writing the prescription for 7 Lovaza capsules per day. As soon as I handed to him, I regretted it. In fact, I am embarassed and angry at myself for having given in.

So I vowed: I will NEVER EVER write another prescription for Lovaza.

I do not believe that we should spread the excessive profiteering of the pharmaceutical industry around on the backs of people who pay their healthcare insurance premiums, just so that a few people, like this selfish couple, can save a few dollars a month.

This is your brain on wheat II

In the original Heart Scan Blog post, This is your brain on wheat, I discussed how opioid peptides (i.e., small proteins that act like opiates such as heroine or morphine) that result from digestion of wheat cause unique effects on the human brain, particularly addictive behaviors. I also briefly reviewed how elimination of wheat has been shown to reduce auditory hallucinations and other psychotic behaviors in a subset of people with paranoid schizophrenia.

These two phenomena, addictions and schizophrenia, are most likely the result of exorphins that cross the blood-brain barrier. Exorphins--exogenous morphine-like compounds--can be blocked by opiate-blocking drugs like naloxone and naltrexone. Naloxone is used in hospitals to reverse morphine or heroine overdoses; naltrexone is being repackaged into a weight loss drug, since blocking wheat-derived exorphins reduces appetite. (Yes: The USDA tells us to eat more wheat, the drug industry sells us the antidote.)

There's another way that wheat can affect the brain and nervous system: immune-activated damage.

This is similar to the effect seen in celiac. There's even overlap with some of the antibody markers used to diagnose celiac, like the anti-gliadin antibodies and the anti-endomysium antibodies.

The most common immune neurological syndrome consequent to wheat consumption is cerebellar ataxia, a condition in which an immune response causes damage to the Purkinje cells of the cerebellum, the portion of the brain responsible for balance and coordination. This results in stumbling, incoordination, incontinence, and eventually leads to reliance on a cane or walker and wearing a diaper. Average age of onset: 53 years. A shrunken, atrophied cerebellum can be seen on an MRI of the brain.

Problem: Most people with central nervous system damage caused by wheat do not have any intestinal symptoms, like diarrhea and abdominal pain, the sort of symptoms usually associated with celiac disease. It means the first sign of wheat-induced brain damage may be bumping into walls and wetting your pants.

There's no such thing as a "no-carb" diet

When I tell patients how I advise a wheat-free, cornstarch-free, sugar-free diet on the background of a low-carbohydrate diet, some people ask: "But can I live on a no-carb diet?"

Well, there's no such thing as a "no-carb" diet. Low-carb, yes. No-carb, no.

Here are the carbohydrate contents of various "low-carb" foods:

Gouda cheese--3 oz contains 1.65 grams carbohydrates
Mozzarella cheese--1 cup contains 2.89 grams carbohydrates
Walnuts--4 oz (56 nuts) contains 2.96 grams carbohydrates
Almonds--4 oz contains 1.38 grams carbohydrates
Sour cream--one-half cup contains 3.31 grams carbohydrates
Red wine--3.5 oz glass contains 2.69 grams carbohydrates
Eggplant--1 cup cooked contains 8.33 grams carbohydrates
Green pepper--1 medium-sized raw contains 5.52 grams carbohydrates
Cucumber--1 medium contains 4.34 grams carbohydrates
Tomato--1 medium contains 4.82 grams carbohydrates

(Nutrition data from USDA Nutrient Database)

In other words, foods thought to be "low-carb" actually contain a modest quantity of carbohydrates.

Such modest quantities of carbohydrates may not be enough to trip your blood sugar. But add up all the "low-carb" foods you consume over the course of a day and you can easily achieve 30 grams or more carbohydrates per day even without consuming any higher carbohydrate foods.

Why doesn't your doctor try to CURE diabetes?

Imagine you have breast cancer. You go to your doctor and she says, "As your pain worsens, we'll help you with pain medication. We'll fit you with a special bra to accommodate the tumor as it grows. That's all we're going to do."

"What?" you ask. "You mean just deal with the disease and its complications, but you're not going to help me get rid of it . . . cure it?"

It would be incredibly shocking to receive such advice. Then why is that the sort of advice given when you are diagnosed with diabetes?

Say you go to the doctor. Lab values show a fasting blood sugar of 156 mg/dl, HbA1c (a reflection of your previous 60 days average glucose) of 7.1%. Both values show clear-cut diabetes.

Your doctor advises you to 1) start the drug metformin, then 2) talk to the diabetic teaching nurse or dietitian about an American Diabetes Association (ADA) diet.

The ADA diet prescribed encourages you to increase carbohydrates and cut fats at each meal and maintain a consistent intake so that you don't experience hypoglycemic (low blood sugar) episodes. You follow the diet, which causes you to gain 10-15 lbs per year, increasing your "need" for diabetes medication. You doctor adds Actos, then Januvia, then injections of Byetta.

Three years and 34 lbs later, you are not responding well to the drug combination with blood sugars rarely staying below 200 mg/dl. You've developed protein in your urine ("proteinuria"), lost 30% of your kidney function, and you are starting to lose sensation in your feet. So the doctor replaces some of your medication with several insulin injections per day.

This formula is followed millions of times per year in the U.S. So where along the way did your doctor mention anything about a "cure"?

Adult diabetes is the one chronic disease that nobody cares to cure. Treat it, maintain control over blood sugars, but cure it? Most physicians say it's impossible.

The tragedy is that diabetes is a curable condition. I've seen it happen many times. Physicians dedicated to curing diabetes like low-carb expert, Dr. Mary Vernon, have cured it countless times. Dr. Eric Westman and colleagues have been building the case for the carbohydrate-restricted cure for diabetes with studies such as this. In this last study, of the 8 participants on insulin + medications at the start of the study, 5 no longer required medications at the close of the study--they were essentially non-diabetic.

I tell patients that diabetes, in fact, is a disease you choose to have or not to have--provided you are provided the right diet and tools. Sadly, rarely are diabetics told about the right diet and tools.

That's why Cadbury Schweppes has been a major contributor to the American Diabetes Association, as are other processed food manufacturers and the drug industry, all who stand to profit from maintaining the status quo.

The cure? Eliminate or at least dramatically reduce carbohydrates, the foods that increase blood sugar.

Note: If you have diabetes and you are taking any prescription agents, such as glyburide, glipizide, insulin, and some others, you will need to discuss how to manage your medications if you reduce carbohydrates. The problem is finding a doctor or other resource to help you do this.

LDL pattern B

Here's a Q&A I stumbled on in the Forum of MedHelp, where people obtain answers from presumed health "experts."

Question:

My VAP test results in July 07 identified an LDL Pattern B.
Overall results:
Total 150
HDL 75
LDL 61
Trig 60
HDL-2 17
LP(a) 6.0
LDL Pattern B

Medications:
Lipitor 10mg
Zetia 10mg
Altace 10mg
Atenolol 50mg
Plavix 75mg
Aspirin 81mg

I had several heart attacks which resulted in CABG performed May 2000. I am a 53 year old white male , 6'1", 190 pounds, exercise every day, watch my diet and feel great. Everything looks OK except my LDL Pattern B. Is there any therapy to improve the Patten B?


Answer from CCF, MD:
Your results indicate an LDL pattern B, which generally indicates small atherogenic LDL particles which may cause increased risk for CAD. However, there are several problems with LDL patterning: 1) its unreliability (of LDL pattern testing ), 2) unclear clinical evidence regarding regarding the usefulness of LDL patterns and particle size. The majority of evidence regarding the progression of atherosclerosis is with LDL lowering and to an smaller extent HDL raising.

All available clinical evidence shows that any particles in the VLDL, IDL, or LDL range are atherogenic, and there is no evidence that whether belonging to pattern A or B one is more atherogenic than others.

Subclass studies have proliferated over the last few years, but many of these studies were funded or subsidized either by suppliers of the assays as a method to expand their use and move them into mainstream practice, or by pharmaceutical companies in an attempt to claim some advantage over other therapeutic agents.
Thus, current data on LDL subclasses are at best incomplete and at worst misleading, suffering from publication bias, and now given the recent results of the Ensign et al. study, unreliable.

Your LDL, and HDL are at goal. The Lpa level is still not clearly linked as a modifiable risk factor for CAD, although elevated levels are now know to be linked to stroke.

Continue with your present treatments: aspirin, plavix, ateonol and altace are all essential medications.



Wow. The extent of ignorance that pervades the ranks of my colleagues is frightening.

Contrary to the response, LDL particle size assays are quite reliable and accurate. I've performed many thousands of lipoprotein assays and they yield reproducible and clinically believable results. For example, eliminate wheat, oats, cornstarch, and sugars and small LDL drops from 2400 nmol/L to 893 nmol/L (NMR)--huge drops. If repeated within a short period of time, the second measure will correspond quite closely.

The data are also quite clear: Small LDL particles (i.e., "pattern B") are a potent predictor of cardiovascular events. What we lack are the treatment trials that show that reduction of small LDL results in reduced cardiovascular events. The reason for this is that small LDL research is not well-funded, since there is no prescription drug to treat small LDL, only nutritional means. Niacin (as Niaspan) is as close as it comes for a "drug" to reduce small LDL. But diet is far more effective.

Given the questioner's fairly favorable BMI of 25.1 and his history of aggressive heart disease, it is virtually certain that he has what I call "genetic small LDL," i.e., small LDL that occur on a genetically-determined basis (likely due to variants of the cholesteryl-ester transfer protein, or CETP, or of hepatic lipase and others).

Ignoring this man's small LDL will, without a doubt, consign him to a future of more heart attacks, stents, and bypass. Maybe by that time the data supporting the treatment of small LDL will become available.

What increases blood sugar more than wheat?

Take a look at these glycemic indexes (GI):


White bread 69
Whole wheat bread 72
Sucrose 59
Mars bar 68
White rice 72
Brown rice 66


I've made issue in past of whole wheat's high GI--higher than white bread. Roughly in the same glycemic league as bread are shredded wheat cereal, brown rice, and a Mars candy bar.

With few exceptions, wheat products have among the highest GIs compared to the majority of other foods. For instance:


Kidney beans 29
Chick peas 36
Apple 39
Ice cream 36
Snickers Bar 40


Yes, by the crazy logic of glycemic index, Snickers is a low-glycemic index food.

While I do not believe that low GI makes a food good or desirable, since low GI foods still provoke high blood sugars, small LDL particles, trigger glycation, and other abnormal phenomena, they are clearly less obnoxious than the items in the first list.

Take a look at this list:

Cornflakes 80
Rice cakes 80
Rice Krispies 82
Rice pasta, 92
Instant potatoes 83
Tapioca 81



Starches that are dried and/or pulverized, such as cornstarch, potato starch, rice starch, and tapioca starch (cassava root) will increase blood sugar even more than wheat. Foods with these starches have GI's of 80-100.

Cornstarch, potato starch, rice starch, and tapioca starch: Sound familiar? These are the main starches used in "gluten-free" foods. A hint of the high GI behavior of these dried starches is seen in the GI for cornflakes of 80.

So remember: Wheat-free is not the same as gluten-free. Gluten-free identifies junk carbohydrates masquerading as healthy because they don't contain one unhealthy ingredient, i.e. wheat.

China fiction?

Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk.

Richard Nikoley of Free the Animal and Stephan Guyenet of Whole Health Source have been talking about an analysis of the China Study raw data performed by a young woman named Denise Minger.

Denise's analysis is nothing short of brilliant, absolutely "must" reading for anyone interested in nutrition.

Her comments on the relationship of wheat to heart disease:

Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?

Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease?

Carbohydrate-LDL double whammy

Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.

The list of reasons why small LDL particles are more atherogenic, i.e., plaque-causing, is long:

--Small LDL particles, being smaller, more readily penetrate the endothelial barrier of the arterial wall.
--Small LDL particles are more adherent to glycosaminoglycans in the artery wall.
--Small LDL particles are poorly taken up by the liver LDL receptor, but enthusiastically taken up by macrophage receptors of the sort in your artery walls.
--Because of their poor liver clearance, small LDL persists in the bloodstream far longer than large LDL.
--Small LDL particles are more oxidation-prone. Oxidized LDL are more likely to trigger inflammatory phenomena and be taken up by macrophages in the artery wall.

Let me add another reason why small LDL particles are more likely to cause plaque: They are more likely to undergo glycation. (More on glycation here.)

Glycation occurs when glucose (sugar) molecules in the blood or tissue modify proteins, usually irreversibly. Small LDL particles are uniquely glycation-prone. (This is likely due to a conformational change of the apoprotein B in the small LDL particle, exposing lysine residues along apo B that become glycated.)

Here's a great demonstration of this phenomenon by Younis et al:


"LDL3" is the small type. Note that small LDL particles are 4-5 times more glycated than large LDL. That's a big difference.

Once glycated, small LDL is especially resistant to being taken up by the liver. Like annoying in-laws, they hang around and hang around and . . . The longer they hang around, they more opportunity they have to contribute to plaque formation.

So, carbohydrates trigger formation of small LDL particles. Once formed, small LDL particles are glycated when blood sugar increases. While LDL can be glycated even when blood sugars are in the normal range (90 mg/dl or less), glycation goes berserk when blood sugars go higher, such as a blood sugar of 155 mg/dl after a bowl of steel-cut oatmeal.

To lose weight, prick your finger

We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day.

So how can you stop triggering insulin?

The easiest way is to eliminate, or at least minimize, carbohydrates. My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket.

Another way is to check your blood sugar one hour after completing a meal and keep your after-eating, or "postprandial," blood sugar 100 mg/dl or less. Let's say you are going to eat stone ground oatmeal, for example. Blood sugar prior to eating is, say, 90 mg/dl. One hour after oatmeal it's 168 mg/dl--you know that this is going to trigger insulin and make you fat. Oatmeal should therefore be eliminated.

Keeping blood sugar to 100 mg/dl or less after eating teaches you how to avoid provocation of insulin. A shrinking tummy will follow.

To do this, you will need:

1) A glucose meter--My favorite is the One Touch Ultra Mini ($13.42 at Walmart). It's exceptionally easy to use and requires just a dot of blood. Drawback: Test strips are about $1 each. Accuchek Aviva is another good device. (We've had a lot of problems with Walgreen's brand device.)
2) Test strips--This is the costly part of the proposition. Purchased 25 or 50 at a time, they can cost from $0.50 to $1.00 a piece.
3) Lancets--These are the pins for the fingerstick device that comes with the glucose meter. A box should be just a few dollars.

No prescription is necessary, nor will insurance pay for your costs unless you're diabetic. To conserve test strips, use them only when a new, untested food or food combination is going to be consumed. If you had two scrambled eggs with green peppers, sundried tomatoes, and olive oil yesterday and had a one hour postprandial glucose of 97 mg/dl, no need to check blood sugar again if you are having the same meal again today.

Iodine update

As the iodine experience grows, I've made several unique observations.

Up to several times per day, I see people who are responding in some positive way to iodine supplementation. (See previous Heart Scan Blog posts about iodine: Iodine deficiency is REAL and The healthiest people are the most iodine deficient.)

Among the phenomena I've observed:

1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development.

2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.

3) Reversal of small goiters also occurs over about 6 months.

4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months.

5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet.

6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures.

7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L.


Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females.

All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.
Why haven't you heard about lipoprotein(a)?

Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

Comments (26) -

  • Matt Stone

    7/1/2010 4:18:14 PM |

    Ah, thyroid normalization. My favorite. Of course, this has a trickle-down effect on DHEA, estrogen, and testosterone as well. Perhaps Lp(a) is one mechanism by which Broda Barnes was able to prevent heart attacks in his patients?  

    http://180degreehealth.com

  • Anonymous

    7/1/2010 4:39:21 PM |

    Aw darn it. Again health info to be confused about. From Taubes' GCBC I read it was apoB supposed to be the one associated with smaller and denser LDL, "the bad LDL", and I thought apoA was the "large and fluffy" or more benign LDL. I'm pretty sure Dr. Lustig says pretty much the same in his "Sugar, the bitter truth" video. There goes my newly acquired "understanding" out the window again.

  • Anonymous

    7/1/2010 4:42:40 PM |

    The last of the 4 treatments doesnt' seem very specific...

    is "T3" a supplement.. if not, how does one go about normalizing the Thyroid?

  • Mike

    7/1/2010 8:12:19 PM |

    That's a lot of fish oil. I take about 1/5 that amount and would find it irritating to have to increase my intake by a factor of 5.

  • Drs. Cynthia and David

    7/1/2010 9:52:19 PM |

    If the pharma industry could actually come up with drugs that work and don't just chase surrogate markers, I'm sure that would be helpful.  I'm all for nutritional and lifestyle fixes, but this won't work perfectly for everyone all the time, so useful drug therapies would be nice too.

    Anonymous, I think you're confusing LDL pattern A and B ("fluffy" vs dense) with apoA and ApoB (HDL associated vs LDL associated proteins).

    Cynthia

  • Anthony

    7/1/2010 10:20:10 PM |

    Dr. Davis,
    How low do you like to see Lp(a)? I've seen recommendations of below 30mg/dl, below 20, and below 10. Mine is 19. Thanks,

    Anthony

  • Dr. William Davis

    7/2/2010 1:12:23 AM |

    Anthony-

    Excellent question . . . for which there's no solid answer.

    Despite all we know about Lp(a), no endpoint data have been generated. However, I can tell you that using particle count measurements in nmol/L a level of 60 nmol/L works very well. In mg/dl, a measure of weight per volume, it depends on the method of measurement used. If the "normal" range is 30 mg/dl or less, then aiming for around 20 mg/dl has worked well.

  • Anonymous

    7/2/2010 1:32:33 AM |

    I asked my cardiologist about it (heads up preventive cardiology at a major research institution in Texas) and he said:

    "Well, there's not anything we can do about it, so why test it?"

  • Anonymous

    7/2/2010 1:55:40 AM |

    My cardiologist and PCP have never ever discussed this with me even though I brought it up for discussion. I think my PCP didn't know much and ignored it. I desperately need a new cardiologist (I live in the SF bay area). Anybody here love their cardiologist and like to share some details? I will be forever thankful Smile

    TIA

  • Paul

    7/2/2010 6:09:32 AM |

    I found this to be a very interesting post over at the Animal Pharm blog concerning this very subject:
    Auto-Tuning Lp(a): Value of Low Carb, High Sat Fat


    They basically come to a very simple conclusion in controlling Lp(a); eat some damn saturated fat! And stay away from the damn carbs!

    Now, let me get back to making my LDL the plain and fluffy kind... someone pass me the ghee please...

  • Harry

    7/2/2010 2:41:24 PM |

    Anonymous and Drs. Cynthia and David, there are several "A" designated particles that frequently get confused. Dr. Davis is talking about lipoprotein(a), with a lower case "a", which consists of an LDL particle with a particle of apolipoprotein(a) attached to it. This apolipoprotein is also designated by a lower case "a". Lp(a) is very atherogenic, and should be minimized.

    Apolipoprotein A, with an upper case "A", on the other hand, is an atheroprotective particle that is a component of HDL. It comes in several varieties. The most plentiful one is designated Apolipoprotein A-I, or Apo A-I, which is the main particle that participates in reverse cholesterol transport, which is the principal way that HDL protects against atherosclerosis, by removing cholesterol from plaque and transporting it back to the liver for disposal. There are also particles designated Apo A-II and Apo A-IV that are also associated with HDL, but their function is not well understood. All the HDL-associated apo A particles are described with the upper case "A".

    Finally, there is the LDL pattern A, which indicates that the LDL particles are mostly large, whereas LDL pattern B indicates that LDL particles are mostly small. These are usually designated with an upper case "A" and "B", and the A pattern is thought to be less atherogenic than the B pattern.

    It is easy to confuse these "A" types, especially Apo A and Apo a, which are two very different particles, the large A apo is good and the small a apo is bad.

  • Kent

    7/2/2010 3:21:25 PM |

    My LP(a) started a year and a half ago at 198 nmol/L, it is now down to 35 nmol/L. Thanks to Dr, Davis's advice that I followed in the Track Your Plaque book, including 4800mg combined EPA, DHA fish oil and 2000mg Niaspan, etc.

    I also want ot mention though that I have been following the Linus Pauling protocol as well, which I believe has a synergistic effect with the other principles applied.

    An interesting thing happened that is worth mentioning, my LP(a) had been gradually dropping over that period of a year and a half from 198 to 45 nmol/L, then I switched to immediate release niacin and my LP(a) jumped back up to 150 nmol/L. That was the only change I made, so I switched back to Niaspan and that is when it went back down to 35 nmol/L.

    Kent

  • Alfredo E.

    7/2/2010 3:35:40 PM |

    Hi All.The following paragraphs were taken from http://www.drlam.com/opinion/Lp(a).asp

    Lipoprotein A, commonly called Lp(a), is a major independent risk factor for cardiovascular disease. The optimum laboratory level should be under 20 mg/dl and preferably under 14 mg/dl.

    Currently, there is no medicine or drugs that to effectively lower your Lp(a). A high Lp(a) is genetically linked. Fortunately, Mother Nature has provided us a much better non-toxic alternative. It consists of large doses of vitamin C, L-lysine, and L-proline.

    Many conventionally trained physician uses niacin to reduce Lp(a). This does work to a limited extend. Niacin reduces the production of lipoprotein A in the liver, and helps to bring down the lipoprotein A in the blood. This is what most conventional doctors use. However, this approach has its limitations because until the endothelial wall is optimized and cleared, the lipoprotein A level will not be able to reduce significantly. The effects of niacin usually hit a plateau after 6-9 months of therapy. If you are on niacin, make sure the liver enzyme levels are taken periodically to make sure the liver is able to handle the high dose of the niacin.

    This last flower:
    Replacing carbohydrates with proteins ignores the fact that protein, once in the intestinal tract, converts to amino acid. Amino acids increase insulin secretion. It is unclear, however, whether proteins are as potent as carbohydrates in stimulating insulin secretion.

    My comment: Is it possible that protein can produce high insulin secretion? So, what is left for simple humans? No carbs, no protein?

  • Anonymous

    7/2/2010 3:52:13 PM |

    Is the LDL carried in the blood by a protein or has it already been oxidized. I'm trying to understand what form chlorestral is in the blood.

  • David

    7/2/2010 6:17:02 PM |

    Alfredo,

    It's true that protein stimulates insulin, but the key is that it doesn't only stimulate insulin. Glucagon, insulin's counter-regulatory hormone, is also stimulated. Insulin secretion  is undesirable in the context of low glucagon (which is what we have with high carbohydrate intake), but it's not such a big deal when the ratio of the two are more balanced (which is what we have with low-carb protein intake).

    David

  • Jack C

    7/3/2010 12:03:08 AM |

    The VAP cholesterol profile, which gives the distribution of LDL and HDL particle sizes a other information, shows an upper limit of 10 mg/dl for Lp(a)cholesterol.

    In recent tests, my wife had an Lp(a) of 6 while mine was 8. Through no fault of our own I might ad.

  • Dr. William Davis

    7/3/2010 12:13:49 AM |

    HI, Kent--

    Great results!

    You are living proof that Lp(a) can indeed be tamed. It sometimes requires some unusual strategies, but huge reductions are possible . . . and Lipitor is not part of the equation.

    Long-term commitment to the effort is the key.

  • Anonymous

    7/3/2010 1:29:29 AM |

    what kind of doctor shoudl i see to get the right tests done.  I know I have high Lipo(a) from a previous test at Mayo.  They recommended that I take drugs and I declined.  Now I'm realizing I don't have the complete story.  I need to know more than just my lipo(a) is high.

    thanks!
    Linda

  • Anonymous

    7/3/2010 6:04:15 AM |

    Hi
    Are there stats on people with lp(a) that don't develop any plaque?
    Also does the same happen with lp(a) as with ldl? that is that is better to have a higher mg/dl with big paricles than a lower mg/dl with small particles?
    Santiago

  • Hans Keer

    7/3/2010 7:28:36 AM |

    I would say apoprotein(a) is normal phenomenon. What is not normal is the abundance of small dense LDL which apoprotein(a) binds to. So the best way to avoid LP(a), is to avoid the abundance of sugars and starch in the diet. All the other (still costing) treatments for Lp(a) won't be necessary then.

  • jd

    7/3/2010 5:39:38 PM |

    Hi,   I recently had a VAP test done via LEF -- I seem to have some very good numbers and some bad LDL ones.  Any comments would be appreciated.

    all values in mg/dl
    LDL 105
    HDL 71
    VLDL 14
    Total Cholesterol 190
    Triglycerides 51
    LP(a) 4.0
    IDL 3
    HDL2 18
    HDL3  53
    VLDL3 8
    LDL1 PatternA 5.4
    LDL2 PatterA 7.5
    LDL3 PatternB 61.6
    LDL4 PatternB 22.4


    LDL Density pattern = B, flagged abnormal

    Vit D  65.4 ng/ml
    Homocysteine 6.2
    C-Reactive Protein 0.2

    I am 55 yr of age, 6'0", 165 lbs, exercise regularly.

    Heart disease in family, mother's father died of heart attack at 66, other 3 grandparents lived into 90s.  father died leukemia cancer 53, mother living at 80 in good health.  Thanks,   Jim

  • Anonymous

    7/7/2010 4:40:46 PM |

    I use Lugols solution 2% and I have absolutely no idea what dosage I should be using.  I have been using one drop about twice a week, but I would like to have a better idea of proper dosage.  Can you help?

  • James L.

    7/13/2010 9:52:15 PM |

    My cardiologist is treating my high Lp(a) with Niaspan, but even with high doses, it has not had much effect. What do you mean by items 3 and 4 on DHEA and T3? Please be more specific. Thanks.

  • Anonymous

    7/29/2010 9:06:55 PM |

    Could you give some dose for T3 and DHEA that you are recommending?

    Thanks!

  • Anonymous

    8/10/2010 8:38:43 AM |

    "If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. "

    Does that mean that high levels of Lp(a) is not inherited from the father?

    Thanks

  • LisaMichelle

    8/24/2011 11:46:03 PM |

    Dear Dr. Davis,

    I'm a 44 yr old female.   I recently had a consultation w/ a cardiologist here in Canada.   I was sent for the consultation because of some strange left jaw and low chest tightness I'd experienced at work the week prior (had been seen then in the ER, normal ECG x 2, normal CXR, normal bloodwork).  Prior to the appt I was told I needed to have fasting bloodwork (so that results were available for the cardiologist to review at my appt).  

    HDL good, LDL good (though at the higher end of the normal range).  Lipoprotein A was 0.55 g/L (which i guess works out to 55 mg/dl which is what the usual unit of measurement is for this one in the U.S.).  The cardiologist told me that all of my bloodwork was normal and that I was very low risk for a heart attack but I requested a copy of my results just to have on file.   I am surprised she didn't mention the elevated Lipoprotein A (normal range for this lab is: 0.00 to 0.33 g/L).   So that got my on my search for info on what exactly Lipoprotein A is, and what it indicates.

    My question is:   I was only told to fast for 12 hours prior to my bloodwork, nothing was said about ensuring I didn't smoke.   Well I did smoke over the 12 hours up until the blood was drawn (even about 30 minutes prior to).   Now I'm reading online that one should not smoke prior to blood being drawn for Lipoprotein A, HDL and LDL, etc.    So could my smoking right up to the time bloodwork done have negatively impacted the results?   Could smoking have made my LDL and Lipoprotein A higher?    Should I have these redone but ensure I don't smoke for 12 hrs prior to blood draw?  (I have a 'quit date' set for next Saturday, so don't worry, I will be quitting).

    Thanks so much,
    Lisa

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