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.
Study review: cerivastatin

Study review: cerivastatin

I'd like to start an occasional series of blog posts on The Heart Scan Blog in which I review studies relevant to the whole heart scan score reversal experience.

In a previous post, Don't be satisfied with "deceleration,"I discussed the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), in which either atorvastatin (Lipitor), 80 mg, or pravastatin (Pravachol),40 mg, was given to 615 women. Both groups showed an average of 15% annual plaque growth, regardless of which agent was taken and regardless of the amount of LDL cholesterol reduction.

I cited another study in which 471 participants received either Lipitor, 80 mg, or Lipitor, 10 mg. The rate of annual score increase was 25-27%, regardless of drug dose or LDL lowering.

Here's yet another study, a small German experience in 66 patients, with a curious design and using the now-defunct statin drug, cerivastatin (Bayccol, pulled in 2001, nearly simultaneous with the publication of this study, due to greater risk of muscle damage, particularly when used in combination with gemfibrozil). Achenbach et al in Influence of lipid-lowering therapy on the progression of coronary artery calcification: A prospective evaluation reported on this trial in which all participants underwent heart scanning to obtain a heart scan score; no treatment was initiated based on the score. A second scan was obtained after the no treatment period, followed by treatment with cerivastatin, 0.3 mg per day. A third scan was finally obtained.

In year one without treatment, the average increase in heart scan scores was 25%. In year two with cerivastatin, the average increase in heart scan score was 8.8%. In 32 participants who achieved LDL<100 mg/dl on the drug, there was an average modest reduction in heart scan scores of 3.7% (i.e., -3.7%).

Now, that was eye-opening. Why did this small study achieve such startlingly different results from the other two studies that showed relentless progression despite even high doses of Lipitor? That remains unanswered. Was cerivastatin unique among statins? Did the unique two-phase trial design somehow change the outcome by triggering participants to change lifestyle habits after their first scan (since most exhibited an increase in score; they were not "blinded" to their scores). Those questions will remain unanswered, since the drug has been made unavailable. This smal l study had actually been intended to be larger, but was prematurely terminated because of cerivastatin's withdrawal.

This experience is unique, as you can see, compared to the two other studies. But it was also smaller. The results are also different than what I have seen in day-to-day practice when I've seen people treated with statin drugs alone (not cerivastatin, of course): rarely do heart scan scores stop increasing. While slowing does usually occur (18-24% per year rates of annual score increase are very common in people who do nothing but take a statin drug and make modest lifestyle changes), I have personally seen only two people stop their score with this strategy alone. Nobody has ever dropped their score taking a statin alone, in my experience.

You can also see the nature of clinical studies: single or limited interventions instituted in order to control for unexpected or complex effects. If three different treatments are used, then what desirable or undesirable effects, or lack of an effect, is due to which treatment agent?

My experience is that no single treatment stops or reduces heart scan scores. It requires a more rational effort that includes 1) identification of all causes of coronary plaque (e.g., low HDL, high triglycerides, Lp(a), small LDL, deficiency of vitamin D, etc, none of which are substantially affected by statin drugs), and 2) correction of all causes. That simple concept has served us well.

Comments (10) -

  • G

    11/27/2007 3:21:00 AM |

    Baychol ('gorilla'-statin when it came out) had a halogenated side group, which means biologically, this gave it 'super' powers.  Other drugs with halogens are also stronger as well (ie topical steroid Clobetasol). Unfortunately, Baychol also had 'super' strong side effects as well! including death from rhabodmyolysis (breakdown of muscle fibers which then leads to 'clogging up' the kidneys when the myoglobins are released into the blood stream, leading to multiple organ failure). Car accident, trauma and marathon runners can get the condition as well.
    I like your scientific method of accurately assessing various dysfunctions of the lipoprotein patterns and correcting with modifications in various strategies (D3, B3, monounsaturated nut oils, etc). Tying this in with tracking the size of shrinking calcium deposits in plaque make a lot of sense (and of course backed up with data, like the one you just posted!)...

    BTW, with erectile dysfunction associated with atherosclerosis, do you also see symptom reversal with the TYP plan? at what level of CAC reversal?  Do you see less use of Viagra later?
    Do you have a cure for white hair too (* ha ha haaaa *)? Global warming?  Amazon de-forestation? You're so humble!
    THANK YOU! G

  • Dr. Davis

    11/27/2007 12:12:00 PM |

    Hi, G--

    As always, thanks for the insights.

    Because 99% of the people who participate in the program begin with asymptomatic coronary plaque, it's not possible to say if symptoms are relieved. The occasional person who chooses this program but has anginal chest pain has indeed experienced complete elimination of symptoms.

    Re: erectile dysfunction. Also, no systematic tracking, so I don't know. Also, I have to admit not purposefully looking for it in men well into the program. But a great thought! It would indeed make sense that restoration of endothelial function and erectile capacity would accompany plaque control and/regression.

  • Anonymous

    11/27/2007 6:00:00 PM |

    Geez Doc, I wish you would have put the last paragraph first on your Blog. I was just about to throw up my hands in despair and call in for a double cheese all meat pizza on wheat, thinking all was lost. I was greatly releived to see I might still make it a while with low dose(10mg)lipitor, 1500 Niacin, Aspirin, and 2000IU D3. With exercise & diet I have worked hard to get LDL,Trigs,LP(a) all in the 30,s. With HDL at 68 I now see hope...don't do that again please!  Over&Out

  • Dr. Davis

    11/27/2007 10:39:00 PM |

    Well, my motivation for posting these occasional summaries of prior clinical studies is to provide, bit by bit, some of the rationale behind the Track Your Plaque program and to show why the simple-minded "take your statin and shut up" approach simply doesn't work.

  • G

    11/28/2007 11:19:00 PM |

    Theoretically, ED and peripheral vascular disease should regress ('cured' perhaps?) if sufficient plaque reversal occurred and original blood flow were restored... wouldn't you think?  ED is frequently common in T2DM and pre-CAD (I made that up) individuals.

    I customarily ask about ED because I use it as a motivating 'factor' in my strategy to get individuals to comply with changes to improve T2DM (yes, I just gave all my secrets now!).  You'd be surprised how effective this strategy is (of course only men -- I use a diff one for females)! Often people will not make necessary changes for 'health' reasons as you know.  The justifications are typically everything-but!  

    You know, I can tell that you're not in the business of selling books, eh?  You're strength is as an innovator imparting knowledge/power...saving lives... preventing unnecessary tragedies...  (THANK YOU FOR ALL YOU DO!)  if you notice improvement in ED, I'd suggest you change your book title to... you know to reach greater target audiences! (well, you'll get the men then you'll have to trust they'll share with their partners)
    'TYP -- Reverses ED and Heart Disease'
    'Don't Live with ED or Coronary Heart Disease'
    'Erectile Dysfunction can be erased, just like your CAD'
    'Better in bed, greater longevity'

    *ha haa haaa* i'm j/k... who is your marketing person?!! not very sexy or splashy... (pardon, if it is you!)

  • bobb

    11/30/2007 6:05:00 AM |

    Dr Davis,

    Two years ago my calcium score was 145.  I am 58 and my score is 294!
    I am very fit, work out 4 times a week with weights and cardio and have for years.  I take 80 mg of vitorin, fish oil, folic acid, nacin, and 2 baby asprin a day. My cholesterol is 142, Hdl 79, LDL 54 and triglycerides 47!  I am 5 9 and 165 lb.  

    Given this I can not seem to stop the increases in calcium.  What else can I do.

    Bill Blanchet is my Doctor!

    Thanks!!

  • Dr. Davis

    11/30/2007 12:38:00 PM |

    Bobb--

    Clearly you can get no more benefit out of squeezing more out of  cholesterol values. I would propose that you and Dr. Blanchet (a refreshingly open-minded physician who I'm going to invite to become a panel member on Track Your Plaque) consider several issues:

    1) Have all causes beyond cholesterol (HDL, LDL, etc.) been identified?

    2) Have you addressed vitamin D? Vitamin D is a huge effect.

    I would invite you to look at our website, www.trackyourplaque.com, for much more information. There is no 10 cent answer to your question. A comprehensive approach that corrects all causes is usually necessary.

  • Neelesh

    12/8/2007 4:30:00 AM |

    I accidentally bumped in to this study about the connection between vitamin D3 and ApoA-I, observing that ApoA-I levels are reduced by Vitamin D3.

    http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=AbstractPlus&list_uids=16236546

    As far as I know, ApoA-I is a good lipoprotein.

    I tried to find some more material on this topic, but to no avail.

    Is this something that you have seen, Dr Davis?

    Thanks!
    -Neelesh
    http://www.recoverytrail.com/blog/

  • Dr. Davis

    12/8/2007 2:00:00 PM |

    Hi, Neeleesh--

    I don't know what to make of this study. It is clearly counter to what I am seeing in real live humans.

    I see the total HDL and the large HDL subclass (richer in ApoA1) increase, often substantially. So I see the exact opposite.

    My observations on this phenomena are informal. Formalizing this observation is part of a future research project.

  • buy jeans

    11/2/2010 8:22:46 PM |

    Those questions will remain unanswered, since the drug has been made unavailable. This smal l study had actually been intended to be larger, but was prematurely terminated because of cerivastatin's withdrawal.

Loading