What Mr. Clinton did NOT do

You've likely already heard that former President Bill Clinton underwent a heart catheterization today during which one of the bypass grafts to his coronary arteries was found to be occluded. The original coronary artery was therefore stented.

Dr. Alan Schwartz, Mr. Clinton's cardiologist, announced to the gathered press that Mr. Clinton had followed a good diet, had adopted a regular exercise program, but that his condition is a "chronic disease" like hypertension that is not cured by these efforts.



Needing a stent just 6 years after four bypass grafts are inserted is awfully soon. I would propose that it has less to do with having a "chronic disease" and more to do with all the things that Mr. Clinton likely is NOT doing. (In addition to all the other things that Mr. Clinton did not do.) In other words, in the Track Your Plaque world, procedures are a rarity, heart attacks virtually unheard of. I would wager that Mr. Clinton has been doing none of the following:

--Taking fish oil. Or, if his doctor was "advanced" enough to have advised him to take fish oil, not taking enough.
--Vitamin D--Followers of the Heart Scan Blog already know that vitamin D is the most incredible health find of the last 50 years, including its effects on reducing heart disease risk. Unless Mr. Clinton runs naked in a tropical sun, he is vitamin D deficient. A typical dose for a man his size is 8000 units per day (gelcap only!).
--Eating a true heart healthy diet. I'll bet Mr. Clinton's doctor, trying to do the "right" thing, follows the prudent course of advising a "balanced diet" that is low in fat--you know, the diet that causes heart disease. Judging by Mr. Clinton's body shape (central body fat), it is a virtual certainty that he conceals a severe small LDL pattern, the sort that is worsened by grains, improved with their elimination.
--Making sure that hidden causes are addressed--In addition to the "hidden" small LDL, lipoprotein(a) is another biggie. Lp(a) tends to be the province of people with greater than average intelligence. I believe Mr. Clinton qualifies in this regard. I would not be at all surprised if Mr. Clinton conceals a substantial lipoprotein(a) pattern, worsened in the presence of small LDL.
--Controlling after-meal blood sugars--Postprandial (after-eating) blood sugars are a major trigger for atherosclerotic plaque growth. There are easy-to-follow methods to blunt the after-meal rise of blood sugar. (This will be the subject of an in-depth upcoming Track Your Plaque Special Report.)
--Thyroid normalization--It might be as simple as taking iodine; it might involve a little more effort, such as supplemental T3. Regardless, thyroid normalization is an easy means to substantially reduce coronary risk and slow or stop coronary plaque growth.


It's not that tough to take a few steps to avoid bypass surgery in the first place. Or, if you've already had a procedure, a few additional steps (of the sort your doctor will likely not tell you about) and you can make your first bypass your only bypass.

Magnesium and arrhythmia

Because magnesium is removed during municipal water treatment and is absent from most bottled water, deficiency of this crucial mineral is a growing problem.

Magnesium deficiency can manifest itself in a wide variety of ways, from muscle cramps (usually calves, toes, and fingers), erratic blood sugars, higher blood pressure, to heart rhythm problems. The abnormal heart rhythms that can arise due to magnesium deficiency include premature atrial contractions, premature ventricular contractions, multifocal atrial tachycardia, atrial fibrillation, and even ventricular tachycardia, fibrillation, and Torsade de Pointes (all potentially fatal). Magnesium is important!

Magnesium supplementation is therefore necessary for just about everybody to maintain normal tissue levels. (The exception is people with kidney disorders, who should not take magnesium without supervision, since they retain magnesium.)

Here is a Heart Scan Blog reader's dramatic rhythm-correcting response to magnesium supplementation:



Dr. Davis,

A few months ago, I contacted you inquiring if you had written any articles on arrhythmia. You were generous enough to answer and guide me to an LEF article you'd written in which you stressed fish oil and magnesium. I had been suffering with bad PVCs [premature ventricular contractions] for over 20 years, and they had gotten so bad recently that I was told my next options were ablation or pacemaker!

I was already on fish oil and had not seen any difference, and so I researched the magnesium you suggested more thoroughly and found a huge body of studies supportng its effect on arrhythmia. I also read many posts on heart forums with people having success with it. After getting advice from various bloggers, I tried magnesium taurate in the morning and Natural Calm (an ionized form of mag citrate) in the afternoon and evening. Within three days the PVCs were quite diminished and by 2 weeks totally gone! As long as I keep taking it, they never return---not even one irregular blip---even when I drink strong coffee! The magnesium also cleared up my restless leg syndrome, my eye twitching, and insomnia. (Apparently, I was the poster-girl for magnesium deficiency.)

I am so angry that after all these years of suffering, trying various medications, and seeing at least 4 different cardiologists that NOT ONE ever even mentioned trying magnesium. The generosity of the few minutes you took to answer my email and steer me in a helpful direction brought me total relief.

Thank you SO MUCH!

Warmly,
Catherine C.

Video teleconference with Dr. Davis


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You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

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Proper use of omega-3 fatty acids/fish oil



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Thinner by Thursday

You want to lose a few pounds . . . Okay, maybe 50 or 75.

Should you exercise? Lengthen you workout? Push the plate away, deny yourself seconds, use a smaller plate?

Of all the weight loss strategies I've tried in patients, there's only one that stands out as a means of obtaining immediate--meaning within 3 days--weight reduction.

Wheat elimination.

Omega-3 Index: 10% or greater?

We've previously considered the question:

What is an ideal level of omega-3 fatty acids in the blood?

Recall that omega-3 levels in red blood cells (RBCs), a measure called the "omega-3 index," have been associated with risk for sudden cardiac death:





In a recent analysis, 265 people experiencing sudden death during a heart attack (ventricular fibrillation, successfully resuscitated) showed an omega-3 index of 4.88%, while 185 people not experiencing sudden death during a heart attack showed an omega-3 index of 6.08%.

We have more ambitious goals than just avoiding sudden death, of course! How about the omega-3 index associated with reduced risk for heart attack? A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks, suggesting that even higher levels are necessary to prevent non-fatal events.

Most recently, another study comparing 50 people after heart attack with 50 controls showed that people with heart attack had an omega-3 index of 9.57% vs 11.81% in controls--even higher. (This study was in a Korean population with higher fish consumption. There was also a powerful contribution to risk from trans fat RBC levels.) The investigators concluded: "The area under the receiver operating characteristic curve of fatty acid profiles was larger than that for traditional risk factors, suggesting that fatty acid profiles make a higher contribution to the discrimination of MI cases from controls compared with modified Framingham risk factors."

The data suggest that, while an omega-3 index of 7.3% is associated with reduced risk for sudden cardiac death, a higher level of 10% or greater is associated with less risk for heart attack. Surprisingly, fish consumption and fish oil intake account for only 47% of the variation in omega-3 index.

I believe the emerging data are becoming increasingly clear: If you desire maximal control over heart health, know your omega-3 index and keep it 10% or higher.

Let's soak 'em with fish oil

If you don't think that charging drug prices for fish oil is wrong, take a look at a letter from an angry Heart Scan Blog reader:


Hello Dr. Davis,

My 44 year old brother had an MI [myocardial infarction, or heart attack] in June. He got pushed around due to "bad government insurance," a state-run program for the "uninsured": government pays 1/3, job pays 1/3, and individual pays 1/3.

What they didn't tell him is that there is no major medical coverage and little to no prescription coverage. We fought for 4 months to get him open heart surgery that the insurance was not going to pay for.

Now, with no assistance, terrible insurance, and no disability he has little to no income. He is a heavy equipment mechanic and is trying to be the "good American"-- take care of his bills, not file bankruptcy, etc.

Anyway, the doctors never seem to pay attention to what they prescribe. Lipitor was not working for him, due to side effects. Now they want to give him Zetia and Lovaza....Zetia at $114, and Lovoza is $169.85! Wow! For dead fish???? I think this is a little fishy! I looked up Lovaza, gee how nice, they will give you a $20 coupon....

Forget it, he can't afford this stuff. So I am enrolling in the Zetia program for him. And trying to get him OTC [over-the-counter] fish oil. The most prevalent fish oil around here (that I take myself is) Omega 3 Fish Oil that has EPA 410mg, DHA 274.

Thanks for your blog. It made me feel better that I wasn't the only one outraged by this stuff. I 've been a nurse for 20 years and it just never seems to get better. Thank you for your wisdom.

Sincerely JP, Tennessee



Had this reader not been aware that her brother could take fish oil as a nutritional supplement, he likely would have been denied the benefit of omega-3 fatty acids in slashing the risk for recurrent cardiovascular events. You and I can buy wonderfully safe and effective fish oil as a nutritional supplement, but there won't be a sexy drug representative to sell it, nor an expensive dinner and payment for a trip to Orlando to hear about it.

Heart scan gone wrong

Those of you reading the Heart Scan Blog, I hope, have come to appreciate the power in measuring atherosclerotic plaque, the stuff of coronary artery disease, and not relying on indirect potential "risk factors," especially the fictitious LDL cholesterol.

However, like all things, even a great thing like heart scans can be misused. Here's a story of how a heart scan should NOT be used, submitted by a reader.


Dr. Davis,

First of all, let me start out by commending you on all of the work you are doing with your website, blogs, etc. You are truly a breath of fresh air at a time when conventional medicine is no longer making any sense. In the last 3 years or so, I have spent a lot of time using the internet to try and find answers . . . and just about every time, when I find things that make "sense," it coincides which the recommendations you provide. Thank You!!

I am 56 years old, and roughly 5 years ago I bought your book, Track Your Plaque, primarily because I had asked my then Internal Medicine physician about why we weren't more "proactive" about determining the state of our cardiovascular health...since the means to do so existed (scans). He was trying to get me to go on a statin because my cholesterol #'s were a little high and at the time I smoked. Other than that, I was in perfectly good health with no side effects or issues. The following year at my annual physical, we again discussed this and he gave me a few options and I ended up having a calcium score done, which showed some blockage, but again, I never had any pains, sweats, or any other symptoms whatsoever, and I am a very active former athlete. This is when I bought your book to try and set a course of plan that wouldn't just include pharmaceuticals.

At the same time, my father was in his last months of life dealing with prostate cancer and the multiple radiation and chemo treatments, so I was making many trips from my home to be with him . . . a 4 hour drive, and very disruptive to family, as I still have 3 kids at home. At what I thought was going to be my last visit with him, I stopped at the cemetery he had planned on being buried to confirm details and such and then started home.

As I was driving, a symptom hit me which I was unfamiliar with (pretty sure it was an anxiety attack now) and I stopped at a friend's house in Chicago, as I didn't want this to be a heart attack while I was driving. This is when I began thinking about the heart scan and the blockage, and ended up driving back later that night and went right to the ER....not because I had any chest pains, but thought it best to be checked out because I did not want to go before my dad did. I ended up staying the night. In the morning the cardiologist PA [physician's assistant] came in with a copy of my calcium scoring and said it was best to have a heart cath...which I was in total agreement with since it would definitively tell me the current condition of my coronary vessels. As I was getting ready to be wheeled into the cath lab, they approached me with a form that would allow them to treat (stent). This is where I became very uncomfortable, in that I had never even met the cardiologist . . . and I didn't like this. No one ever had asked if I was experiencing pains or anything else . . . but I buckled and signed the form.

Before you knew it, I was awake watching my heart being cathed and the cardiologist angry because they did not have all the right sizes of stents, so he had to use a couple extra and I ended up w/5 total . . . and my life changed forever! In looking back, I can't necessarily argue the need for intervention, but in hindsight, it would have been nice to have tried an alternative method of reversing my plaque, especially since I had never experienced any symptoms and didn't appear to be in any imminent danger.

Upon release from the hospital I was put on a cocktail of drugs that typically follow and I then began to search and research. No one talked to me about lifestyle changes other that smoking....but nothing on diet or other means of cholesterol control, etc....in fact, when I had to pick out my meals in the hospital, they wouldn't let me have cheese....but the rice crispy treat was fine....how stupid! They originally told me the Plavix had to last 6 months....and then 12....and then 2 years....I stayed on it for 1-1/2 years and it was the only thing other than a baby aspirin. I went to another cardiologist out of town and he wanted me back on 5 or 6 medications and said that now I had the stents....I would have to be on these for life.....and he was the expert that talked at several main conferences.....my last trip to him.

Now, fast forward to about 6 months ago: I was participating in a father-son soccer scrimmage and was playing goalie. It was wet out and I couldn't catch very well. So being the competitive person I am, I resorted to using my chest on several of the saves and also took a direct blow to my eye ( I wear glasses) and the eye started swelling up pretty good. We then finished and went inside to have pizza and everyone was concerned about my eye. About 30 minutes later I excused myself as i felt some pretty significant sweats and subsequently a pretty severe pain directly in the middle of my chest....I was having a heart attack! Called 911 and went to hospital (2-1/2 years since original stents) and my local cardiologist removed the blockage that was at the anterior portion of my 1st stent causing the blockage. The huge disappointment to me is that I had taken many steps to improve my overall health. But now that I have foreign bodies in my vessels, the chance of further clotting is something that i will most likely always have to live with.

BU, Michigan



This is an example of how heart scans should NOT be used. They should NEVER be used to justify a procedure, no matter how high the score or where the plaque is located. The "need" for procedures is determined by symptoms (BU's symptoms were hardly representative of heart disease), blood findings, EKG, stress testing, and perhaps CT coronary angiography. "Need" for procedures can never be justified simply on the basis of the presence of plaque by a heart scan calcium score.

Unnecessary procedures like the one BU underwent are not entirely benign, as his experience at the soccer game demonstrated.

Heart scans are truly helpful things. But, like many good things, they are subject to misuse in the hands of the uncaring or greedy.

Blood sugar: Fasting vs. postprandial

Peter's fasting blood glucose: 89 mg/dl--perfect.

After one whole wheat bagel, apple, black coffee: 157 mg/dl--diabetic-range.

How common is this: Normal fasting blood sugar with diabetic range postprandial (after-eating) blood sugar?

It is shockingly common.

The endocrinologists have known this for some years, since a number of studies using oral glucose tolerance testing (OGTT) have demonstrated that fasting glucose is not a good method of screening people for diabetes or pre-diabetes, nor does it predict the magnitude of postprandial glucose. (In an OGTT, you usually drink 75 grams of glucose as a cola drink, followed by blood sugar checks. The conventional cut off for "impaired glucose tolerance" is 140-200 mg/dl; diabetes is 200 mg/dl or greater.) People with glucose levels during OGTT as high as 200 mg/dl may have normal fasting values below 100 mg/dl.

High postprandial glucose values are a coronary risk factor. While conventional guidelines say that a postprandial glucose (i.e., during OGTT) of 140 mg/dl or greater is a concern, coronary risk starts well below this. Risk is increased approximately 50% at 126 mg/dl. Risk may begin with postprandial glucoses as low as 100 mg/dl.

For this reason, postprandial (not OGTT) glucose checks are becoming an integral part of the Track Your Plaque program. We encourage postprandial blood glucose checks, followed by efforts to reduce postprandial glucose if they are high. More on this in future.

Diabetes from fruit

Mitch sat in my office, looking much the same as he had on prior visits.

At 5 ft 7 inches, he weighed a comfortable 159 lb, though he did have a small visible "paunch" above his beltline.

I had been seeing Mitch for his heart scan score of 1157 caused by low HDL of 38 mg/dl, severe small LDL (87% of total LDL), and lipoprotein (a).

Part of Mitch's therapeutic program was elimination of wheat, cornstarch, and sugars, the three most flagrant triggers of small LDL particles, and weighing his diet in favor of oils and fats to reduce Lp(a). However, Mitch somehow failed to follow our restriction on fruit, which we limit to no more than two 4 oz servings per day, preferably berries. He thought we said "Eat all the fruit you want." And so he did.

Mitch had a banana, orange, and blueberries for breakfast. For lunch, along with some tuna or soup, he'd typically have half a melon, a pear, and red grapes. For snacks, he'd have an apple or nectarine. After dinner, it wasn't unusual for Mitch to have another piece of fruit for dessert.

Up until Mitch's last visit, he'd had blood glucose levels of 100-112 mg/dl, above normal and reflecting mild insulin resistance and pre-diabetes. Today, on his unlimited fruit diet, his blood sugar: 166 mg/dl--well into diabetes territory.

I helped Mitch understand the principles of our diet better and advised him to reduce his fruit intake to no more than the 2 small servings per day, as well as sticking to our "no wheat, no cornstarch, no sugar" principles.

While fruit is certainly better than, say, a half-cup of gummy bears (84.06 g carbohydrates, 50.12 g sugars), fruit is unavoidably high in carbohydrates and sugars.

Take a look at the carbohydrate content of some common fruits:

Apple, 1 medium (2-3/4" dia)
19.06 g carbohydrate (14.34 g sugar)

Banana, 1 medium (7" to 7-7/8" long)
26.95 g carbohydrate (14.43 g sugar)

Grapes, 1 cup
27.33 g carbohydrate (23.37 g sugar)

Pear, 1 medium
25.66 g carbohydrate (16.27 g sugar)

Source: USDA Food and Nutrient Database

Fruit has many healthy components, of course, such as fiber, flavonoids, and vitamin C. But it also comes with plenty of sugar. This is especially true of modern fruit, the sort that has been cultivated, hybridized, fertilized, gassed, etc. for size and sugar content.

When you hear such conventional advice like "eat plenty of fruits and vegetables," you should hear instead: "eat plenty of vegetables. Eat a small quantity of fruit."

The sniff test

It is well established that omega-3 fatty acids from fish oil are free of mercury, PCBs, furans, and other pesticide residues. Several independent analyses have all agreed: little to none are contained in fish oil. In the Consumer Lab series of assessments, for example, no fish oil supplement failed because of any heavy metal or pesticide residue.

However, oxidative byproducts are a problem. Just as fish that sits on the store shelf or your refrigerator too long starts to smell "fishy," so will fish oil. When fish or fish oil becomes rancid, smelling like rotten fish at its worst, it means that
No flush = No effect

No flush = No effect



"Inositol Hexanicotinate is the true 'flushless niacin.' Unlike 'sustained-release' niacin, which is just regular niacin in a pill which dissolves more slowly, Inositol Hexanicotinate is a niacin complex, formed with the B-vitamin-like inositol. When you take an IHN supplement, the central inositol ring gradually releases niacin molecules, one at a time delivering true niacin. This, like “sustained-release” niacin, allows you to take niacin at clinically-proven doses without going crazy with the itch."


That above bit of nonsense adorns one manufacturers sales pitch for its no-flush niacin. No-flush niacin is one of the biggest scams in the health food store.

Ordinarily, I love health food stores. There's lots of fun and interesting things available that pack real power for your health program. Unfortunately, there's also outright nonsense. No-flush niacin is absolute nonsennse.

No-flush niacin is inositol hexaniacinate, or an inositol molecule complexed with 6 niacin molecules. So it really does contain niacin. However, although it works in rats, it exerts no known effect in humans.

Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

The lack of any observable effect and no studies whatsoever showing a positive effect (there is one study demonstrating no effect), manufacturers continue to manufacture it and health food stores continue to push it as an alternative to niacin that causes the flush. It's quite expensive, commonly costing $30-$50 for 100 tablets.

Don't fall for this gimmick. Niacin is among the most helpful of treatments for gaining control over coronary plaque. It raises HDL, corrects small LDL, reduces triglycerides (along with its friend, fish oil, of course), reduces lipoprotein(a), and dramatically contributes to reduced heart attack risk. No-flush niacin does none of this. Track Your Plaque Members: For a thorough discussion of niacin--how to use it, what preparations work and which do not, read Niacin: Ins and outs, ups and downs on the www.cureality.com website.

Comments (3) -

  • Hoop

    7/4/2007 8:38:00 AM |

    Then again it maybe this patient was using too low a dose?
    And what else was the patient ingesting? And there is the issue of which class lipid abnormality this patient had.

    In my comments below I've included some abstracts of some human based studies that suggest inositol hexanicotinate isn't useless for altering serum lipid levels.


    If we assume for a moment the validity of your anecdote,
    I won't call inositol hexanicotinate worthless rather I would suggest it might have has narrower scope of uses not including the altering
    blood lipids.  Not everyone (me) takes large doses niacin for it lipid altering properties. Consider Kaufman's work with niacinamide in patients
    with degenerative arthritis. He used doses of 1.5 to 4 grams and
    claimed increased joint mobility after a couple of months.
    In my experience, niacin also works as well as niacinamide
    against my pains in and around my joints. Its benefits against the pain come about gradually but
    nonetheless are quite effective for me.

    The flush can be pretty nasty if one isn't careful about the dose.
    I know when I mixed niacinamide and niacin in the past I seemed
    to have somewhat more flushing. I took niacin for several years
    until it started to be trigger atrial premature beats.
    I'll comment further in this posting on a way around these adverse effects of niacin.


    Inositol hexanicotinate maybe superior provided one chooses
    the right patients? Please see the second abstract below.
    ----------------------------------------------------


    1: Eur. J. Clin. Pharmacol. 1979 Aug;16(1):11-5.


    Nocturnal inhibition of lipolysis in man by nicotinic acid and derivatives.


    Kruse W, Kruse W, Raetzer H, Heuck CC,
    Oster P, Schellenberg B, Schlierf G.


    The effect of nicotinic acid and several derivatives
    on the nocturnal level of free fatty acids was studied
    in 12 healthy young women and men. Free fatty acids
    are an important precursor of plasma triglycerides
    and their concentration is highest at night.
    The drugs used were nictinic acid, beta-pyridyl-carbinol,
    mesoinositol hexanicotinate and xantinol nicotinate.
    The highest plasma nicotinic acid level was observed
    with beta-pyridyl-carbinol, but significant reduction in
    free fatty acids during the entire night was only
    achieved with inositolhexanicotinate and
    xantinol nicotinate. There was no correlation between
    the plasm levels of free fatty acids and nicotinic
    acid at any sampling time. If prolonged reduction
    in free fatty acid concentration is desired in the therapy of
    hyperlipidemias, the inositol and xantinol esters of
    nicotinic acid appear to be superior to the other preparations.


    PMID: 499296 [PubMed - indexed for MEDLINE]
    ========================================


    Inositol hexanicotinate seems to work to lower some
    blood lipids in this next human study and granted
    another drug is also involved.
    -------------------------------------------------------------
    1: Arzneimittelforschung. 1979;29(10):1621-4.


    [Treatment of various types of hyperlipoproteinaemia with
    a combination of Mg-chlorophenoxy-isobutyrate and
    mesoinositol-hexanicotinate (author's transl)]


    [Article in German]


    Bolzano K, Krempler F, Haslauer F.


    50 patients with different types of hyperlipoproteinaemia
    were treated with a combination of Mg-chlorophenoxyisobutyrate
    (700 mg) and mesoinositol-hexanicotinate (500 mg) (Atroplex)
    twice daily. 7 patients had type IIa, 39 patients type IIb
    or IV and 4 patients type V. After a period of one
    month without any treatment the patients were treated
    during two months. While the effects of this combination
    on cholesterol of type IIa patients was poor, the
    drug had an excellent lipid-lowering effect in the patients
    with type IIb, IV and V. After 14 days' treatment the
    plasma cholesterol and triglyceride levels in
    patients of type IIb or IV were significantly lowered.
    This effect became even more pronounced after
    one-month treatment. There was no significant difference
    between the effect of one-month treatment and
    that of two-month treatment. About two-thirds of the
    patients of type IIb or IV were responders. No serious side
    effects could be observed during our study.


    Publication Types:
        English Abstract


    PMID: 583231 [PubMed - indexed for MEDLINE]
    --------------------------------------------------
    So could it have been that this patient had one of the classes
    of hyperlipidemic disorders such as type 1, type
    2-a or type 3 for which inositol hexanicotinate
    maybe ineffective?


    =====================================================
    It may have other uses see next paper.
    -------------------------------------


    1: Clin. Rheumatol. 1988 Mar;7(1):46-9.


    A double blind randomised placebo controlled trial
    of hexopal in primary Raynaud's disease.


    Sunderland GT, Belch JJ, Sturrock RD,
    Forbes CD, McKay AJ.


    University Department of Surgery,
    Glasgow Royal Infirmary, Scotland.


    The peripheral vasospastic symptoms associated
    with Raynaud's disease continue to
    be an unsolved clinical problem. Hexopal
    (Hexanicotinate inositol) has shown
    promise in uncontrolled studies and its use in
    patients with Raynaud's disease may reduce such
    vasospasm. This study examines the effects of
    4 g/day of Hexopal or placebo, during cold weather,
    in 23 patients with primary Raynaud's disease.
    The Hexopal group felt subjectively better and
    had demonstrably shorter and fewer attacks of
    vasospasm during the trial period.
    Serum biochemistry and rheology was
    not significantly different between the
    two groups. Although the mechanism of
    action remains unclear Hexopal is safe
    and is effective in reducing the vasospasm
    of primary Raynaud's disease during the winter months.


    Publication Types:
        Clinical Trial
        Randomized Controlled Trial
        Research Support, Non-U.S. Gov't


    PMID: 3044673 [PubMed - indexed for MEDLINE]
    ====================================================
    : J. Int. Med. Res. 1979;7(6):473-83.


    An experimentally controlled evaluation of the effect
    of inositol nicotinate upon the digital blood flow
    in patients with Raynaud's phenomenon.


    Holti G.


    The vaso-active effects of inositol nicotinate (Hexopal)
    were investigated in thirty patients with primary and
    secondary Raynaud's phenomenon using several
    non-invasive experimental techniques under
    controlled conditions. The earlier formed impression
    that this drug requires a prolonged 'build-up' period was
    confirmed. Recording the time required to induce
    Raynaud's phenomenon as well as assessments of total
    and nutrient digital blood flow showed significant
    beneficial therapeutic effects upon the skin's
    microcirculation by inositol nicotinate. This study
    suggests that the therapeutic effect of this drug is not
    merely due to vasodilation but that other mechanisms
    such as enhanced fibrinolysis and lowering of
    serum lipids may play a significant part in its
    overall effect. Smokers responded slower than non-smokers,
    but even elderly patients with longstanding vasospastic
    disease showed measurably improved digital circulation.
    Unlike some other drugs in this field inositol nicotinate was found
    to be effective orally and to be devoid of unwanted side-effects.
    However, in the majority of patients it failed to
    abolish their increased vascular spasm although
    it diminished it significantly in most. It appears
    to be a safe and well tolerated drug, which,
    together with other symptomatic measures, merits
    to be used in the management of vasospastic
    disease of the extremities even in the
    presence of partial obliteration of the microcirculation.


    Publication Types:
        Clinical Trial
        Randomized Controlled Trial


    PMID: 391622 [PubMed - indexed for MEDLINE]
    =======================================


    Perhaps what is needed is a larger dose in comparison
    to other forms of niacin?

    ---------------------------------------------
    Now to expand the topic to plain old TR niacin and betaine.
    ---------------------------------------------

    Timed release niacin as I recall is twice a effective
    as simple niacin in lowering lipids and twice as toxic.
    So it seems come out about even if one takes a half
    the dose of TR niacin.

    Of course, what I'd love to test is niacin in its various forms
    along with trimethylglycine (TMG) aka betaine. And I won't  
    just consider lipid level effects but also the effects on
    osteoarthritis and other joint pains.

    Why do I mention betaine? I know from personal experience
    high doses of betaine along with niacin pretty well blocks
    the flushing effect as well as completely
    blocking the atrial premature beats (AVB) that I would get
    when taking either high dose niacin or niacinamide.
    I had taken niacin at a rather high doses for about 5 or 6 years
    back a couple of decades ago and then I started
    to get the AVBs when I tried to
    resume the use of doses above 100 milligrams.
    Now of course provided I take the betaine I don't have
    this problem. However, I do get AVBs if I don't use the
    betaine and only take the niacin.
    Granted some suggest niacin lowers the lipid levels
    by "stressing" the liver so if betaine blocks
    this effect it maybe contraindicated for the purpose
    of changing lipid levels.
    Here are Pubmed ID numbers, for some papers that
    reflect similar thinking using betaine to reduce
    the toxicity of high dose B-3.
    PMID: 10985907
    PMID: 17156888

    --------------------------------------------

    I'd be interested in your comments on the points of
    theory and science. I am not looking for personal
    advice. A number of people including myself
    are discussing the niacin topic on the
    Usenet forum....sci.life-extension (which
    is also available by way of the Google Group
    Archive for free provided you have a throw away email address).
    Someone else referred to your blog comments and yet
    another person proposed contacting you for a comment.
    I was elected Wink to contact you.
    The group/forum members were interested as to whether there is
    more to your anecdote concerning the possible ineffectiveness
    of inositol hexanicotinate as a lipid lower agent.

    Thank You.

  • Dr. Davis

    7/4/2007 1:36:00 PM |

    Thanks for your insightful comments.

    My experience is based on the experiences of about 10 patients on the no-flush preparation in doses of 1000-4000 mg per day.

    If the rationale for the no-flush preparation is that it provides niacin in such a way as to avoid the flush, we should see rises in HDL, reductions in triglycerides, small LDL, and lipoprotein(a), regardless of the type of hyperlipidemia present (IIa, IIb, III, etc.).

    After using no-flush for up to one year, I have seen absolutely no effect, accepting my relatively small experience.

    Please also understand that my focus is prevention and reversal of coronary heart disease, something that the Track Your Plaque approach does exceptionally well, so I try not to stray off too far from our focus. But why would no-flush have any beneficial effects on arthritis, etc.,as an alternative method of delivering niacin when niacin itself does not possess these effects? I'm not sure I follow the rationale. To be included in a program of coronary atherosclerotic regression, we would have to see substantial effects, as we do with plain old niacin.

    Nonetheless, I encourage your continuing interesting thoughts.

  • buy jeans

    11/3/2010 12:29:51 PM |

    Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

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