Getting your dose of fish oil right

Confusion often stems from the simplest of calculations: dose of fish oil.

Actually, you and I don't take fish oil for fish oil. We take fish oil for its content of omega-3 fatty acids, the dominant ones being EPA and DHA. The contents of fish oil outside of its EPA + DHA content likely exert little or no benefit (beyond that of other dietary oils).

To determine what you are currently taking, simply examine the back of your fish oil bottle and look for the EPA + DHA composition. This should be clearly and prominently labeled. If not, don't buy that brand again. Add up the EPA + DHA content per capsule, then multiply by the number of capsules you take per day. That yields your daily EPA + DHA intake.

The only other substantial source of omega-3 fatty acids is fish. Other food sources, such as non-fish meats, eggs, etc., contribute little or none. Processed foods that bear health claims of "contains heart healthy omega-3" often contain linolenic acid or flaxseed oil, which contributes very little to total EPA + DHA, or contain relatively trivial quantities of DHA. What are you doing eating processed foods, anyway?

What should the total daily dose of EPA + DHA dose be? That depends on what your goals are.

If your goal is to modestly reduce the risk of dying from heart attack, then just eating fish a couple of times per month will begin to exert an effect, or just taking a dose of 300 mg EPA + DHA per day from a low-potency capsule will do it. However, that's an awfully unambitious goal.

Our starting omega-3 dose in the Track Your Plaque program has, over the years, increased and now stands at 1800 mg EPA + DHA per day. However, the dose for 1) full reduction of triglycerides and/or triglyceride-containing abnormal lipoproteins, 2) reduction of Lp(a), and 3) the ideal dose for coronary and carotid plaque control are substantially higher.

But once you know your desired daily target of total EPA + DHA, you can easily determine the quantity of capsules to take by doing the above arithemetic, totaling the EPA + DHA per capsule. For example, if you have been instructed to take 6000 mg per day EPA + DHA, and your capsule contains 750 mg EPA + DHA, then you will need to take 8 capsules per day (6000/750).

Flat tummy . . . or, Why your dietitian is fat

When I go to the hospital, I am continually amazed at some of the hospital staff: 5 ft 4 inch nurses weighing over 200 lbs, etc.

But what I find particularly bothersome are some (not all) hospital dietitans--presumably experts at the day-to-day of healthy eating--who waddle through the halls, easily 40, 50, or more pounds overweight. It is, to say the least, credibility-challenging for an obese dietitian to be providing nutritional advice to men or women recovering after bypass or stent while clearly not in command of nutritional health herself.

What's behind this perverse situation? How can a person charged to dispense "healthy" nutritional information clearly display such clear-cut evidence of poor nutrition?

How would you view a success coach dressed in rags? Or a reading coach who can barely read a sentence?

Easy: She follows her own advice.

Hospital dietitians are essentially forced to adhere to nutritional guidelines of "official" organizations, such as the American Heart Association and the USDA. There is some reason behind this. Imagine a rogue dietitian decides to advocate some crazy diet that yields dangerous effects, e.g., high-potassium diets in people with kidney disease. There is a role for oversite on the information any hospital staff member dispenses.

The problem, of course, doesn't lie with the dietitian, but with the organizations drafting the guidelines. For years, the mantra of hospital diets was "low-fat." More recently, this dated message has begun--only begun--to falter, but now replaced with the "healthy, whole grain" mantra. And that is the advice the hapless dietitian follows herself, unwittingly indulging in foods that make us fat.

Sadly, the "healthy, whole grain" message also contributes to heart disease via drop in HDL, increased triglycerides, a huge surge in small LDL, rise in blood sugar, increased resistance to insulin, tummy fat, and diabetes. Yes, the diet provided to survivors of heart attack increases risk.

The "healthy, whole grain" message also enjoys apparent "validation" through the enormous proliferation of commercial products cleverly disguised as healthy: Cheerios, Raisin Bran, whole grain bread, whole wheat pasta, etc. The "healthy, whole grain" message, while a health disaster, is undoubtedly a commercial success.

I'll bet that our fat dietitian friend enjoys a breakfast of healthy, whole grains in skim milk, followed by a lunch of low-fat chicken breast on two slices of whole grain bread, and ends her day with a healthy meal of whole wheat pasta. She then ascribes her continually climbing weight and size 16 figure to slow metabolism, lack of exercise, or the once-a-week piece of chocolate.

Wheat has no role in the Track Your Plaque program for coronary plaque control and reversal. In fact, my personal view is that wheat has no role in the human diet whatsoever.

More on this concept can be found at:

What's worse than sugar?

The Wheat-Deficiency Syndrome


Nutritional approaches: Large vs. Small LDL

Are you wheat-free?

Statin drug revolt

I sense a growing revolt against the intrusion of statin drugs into our lives.

No doubt, the statin drug industry is, at least from an economic perspective, a huge success: $27 billion annual revenues at last accounting. The latest big plug for more and more statins was the JUPITER trial that showed reduced cardiovascular events on Crestor in people with "normal" LDL cholesterol levels and increased c-reactive protein.

It seems that not one day passes that doesn't include some news story about the "benefits" of statin drugs: reduction in heart attack, stroke, colon cancer, osteoporosis, heart failure, etc.

Ironically, the overwhelming economic success of the statin drug industry also seems to be encouraging a grassroots revolt.





More and more people are coming to the office, more people commenting on the web over how they want to avoid statin drugs, stop a drug they are already taking, or at least reduce the dose of an ongoing drug.

My day-to-day experience with coronary plaque control and reversal is that, while statin drugs are helpful tools, they are not necessary tools for full benefit of a prevention program. "Need" for statin drugs can differ by the patterns measured, though not the usual patterns suggested by the drug industry. For instance, using C-reactive protein, a la JUPITER, as justification for statin prescription is, in my view, totally absurd and makes no sense whatsoever, since inflammatory responses can be effective reduced with plenty of other strategies besides statin drugs. Conventional LDL, likewise, is a fictitious number that often bear little or no resemblance to the true and genuine measured value (apoprotein B or LDL particle number).

So here are a number of strategies that can help reduce or eliminate the "need" for a statin drug:

--Elimination of wheat and cornstarch--This is no namby-pamby dietary strategy, as low-fat diets were. This is a powerful, enormously effective strategy, particularly if LDL is in the small category. Small LDL drops like a stone when these foods are eliminated. This means no breads, pasta, breakfast cereals, pretzels, crackers, chips, tacos, wraps, etc.
--Non-wheat fibers--Especially raw nuts, ground flaxseed, and oat bran.
--Vitamin D restoration
--Fish oil
--Weight loss
--Niacin

There are additional strategies that focus on specific subsets of LDL cholesterol (e.g., Lp(a) masquerading as LDL). But the above list can reduce LDL cholesterol substantially, reducing the apparent "need" for a statin drug.

You will notice that there are few money makers in the above list, compared to the billions of dollars reaped by the statin drug industry. There is therefore little incentive to allow a pretty sales rep to go to your doctor and pitch the use of over-the-counter vitamin D or make changes in diet.

Statin drugs in my view need to be shoved back into their more limited role as drugs to be used on occasion when necessary (e.g., heterozygous familial hypercholesterolemia with LDL cholesterol values of 250 mg/dl in a person with measurable coronary plaque). These should never have achieved the "celebrity" status they enjoy, complete with gushing endorsements by TV personalities, daily news stories, and back-to-back TV commercials.

Join the revolt!

Lovaza Rip-off

Lovaza is GlaxoSmithKline's prescription fish oil, an ethyl ester modification to allow higher concentration of omega-3 fatty acids, EPA + DHA, per capsule. Each capsule contains 840 mg EPA + DHA.

It is FDA-approved for treatment of high triglycerides (>500 mg/dl). In their marketing, they claim "Unlike LOVAZA, dietary supplements are not FDA approved to treat any disease." They also highlight the "patented five-step" purification process that eliminates any concerns over mercury or pesticide residues.

What does Lovaza cost? In Milwaukee, it costs about $70 per capsule per month (PCPM). Most people are taking four capsules per day: $280 per month, or $3360 per year to obtain 3360 mg of EPA + DHA per day. (Funny coincidence with the numbers.)

Did you catch that? $3360 per year, just for one person to take Lovaza.

What if I instead went to Costco and bought their high-potency fish oil. This is also an ethyl ester form. It costs $14.99 for 180 capsules, or $2.50 PCPM; each capsule contains 684 mg EPA + DHA. I would therefore have to take five capsules per day to obtain the same 3360 mg EPA + DHA per day. This would cost me 5 x $2.50 = $12.50 per month, or $150 per year.

$3360 per year vs. $150 per year to obtain the same dose of omega-3 fatty acids, or a 22.4-fold difference.

Lovaza is FDA-approved for treatment of high triglycerides. But I am seeing more and more people take it for other reasons at this four-capsule-per-day dose. Regardless, this "drug" is adding $3360 per year costs to our healthcare. A school teacher, for instance, recently commented to me that she didn't care about the costs, since her insurance (in Milwaukee county, teachers have unbelievably generous healthcare coverage) covers Lovaza. I've heard this from others: insurance covers it, so they don't care how much it costs.

Guess who eventually has to pay the $3360 per year per person costs? Yup, you and me. We all bitch and moan about the costs of healthcare and health insurance, but many of us are more than willing to shift the costs to our friends and neighbors to save a few bucks. You think Lipitor makes a bundle of money for Pfizer at about $120 per month? Lovaza is making a bundle of money for GlaxoSmithKline, and all because people are cheap and willing to selfishly shift costs to other people.

Keep in mind that $3360 per year is just for fish oil. It's not for surgery, it's not for hospital care, it's just for stinking fish oil.

Santa Claus is alive . . . and works for the drug industry



Maybe your teenagers no longer believe in Santa Claus, but I assure you: Not only is he alive, I believe that we have evidence that he works for the drug industry!

Psshaww! you say. Yet another rant from that kook, Davis. Who can he pick on next? What other imagined "conspiracies" can he uncover?

Let me recount the evidence and I'll let you decide how damning it all is:

--Christmas is a culture of excess, overeating, celebration: Cookies, candy canes, pie, chocolate, egg nog, more cookies . . . A virtual wheat and sugar frenzy!

--Wheat and sugars make us diabetic!

--What does a diabetic look like? How about big protuberant abdomen, florid cheeks, baggy eyes (from sleep apnea)? The red outfit and beard is optional, of course. Could you think of a better representation of what happens to a person when they eat goodies all the time?


I therefore submit that Santa Claus is at the root of a campaign to cultivate diabetes! Diabetes: a growth industry that is raking in billions of dollars for the drug companies!

I'd bet that Mr. Claus would agree with the dietary advice dispensed by the folks at the American Diabetes Association website:

A place to start is at about 45-60 grams of carbohydrate at a meal. You may need more or less carbohydrate at meals depending on how you manage your diabetes.


Eat more carbohydrates, get fatter in the abdomen, require more medication to keep sugar low. Then start over: eat more carbohydrates, get fatter, more medicines. Kaching!

"You may need more?" Personally, I'd be rendered comatose and helpless if I indulged in such carbohydrate gluttony.

If Mr. Claus were, instead, interested in our health and keeping us non-diabetic, Christmas would be a time for pistachios, almonds, dark chocolates, and tea.

You want health advice? Don't ask Santa Claus!

Another case of aortic valve disease reduced with vitamin D

I watched Seth's aortic valve deteriorate over a two year period.

I was first consulted in 2004 to offer an opinion on Seth's heart scan score of 779 and flagrantly abnormal cholesterol patterns, including triglycerides in the 400 mg/dl range. But I heard a murmur, as well, a murmur of a leaky aortic valve, "aortic valve insufficiency."

Over the next two years, I watched Seth's aortic valve worsen, going from mild leakiness to severe.

In 2006-2007, I tiptoed into vitamin D replacement and asked Seth to add some vitamin D. Time passed and Seth's aortic valve got progressively worse.

Over the past year, However, he's maintained a truly healthy level of vitamin D, with blood levels consistently in the 60-70 ng/ml range.

While Seth's last echocardiogram showed a severely leaky aortic valve, the most recent echo showed mild leakiness ("mild aortic insufficiency")--a dramatic reduction.

I continue to see this in many, though not all, patients with aortic valve disease. Though I've more frequently witnessed either stalled progression or reversal of aortic valve stenosis (stiffness), I've now seen a handful of people with aortic valve leakiness (insufficiency) also reverse.

I've posted about this peculiar phenomenon previously:

Aortic valve disease and vitamin D
More on aortic valve disease and vitamin D

Prior to vitamin D, I had NEVER witnessed any aortic valve disease stop or reverse.

A formal trial at some point would be invaluable.

Track Your Plaque Program Data Tracking Tools

At last: After talking about the new Track Your Plaque community tools for the last year, our data tracking software is now available!



Track Your Plaque is, admittedly, somewhat data-intensive. The basic concept relies on the fact that we track heart scan scores, cholesterol values, lipoprotein values like percent small LDL and Lp(a), vitamin D blood levels, intake of omega-3 fatty acids, etc. Our new data tracking tools will help Members track their data over time.

Even more interesting, you can allow other Members (not required) to view your data for comments and feedback. You can also view the program data of other Members (if they choose to make their data "public") to learn how they are going about stopping and reversing their coronary plaque.

In other words, our graphic data tracking tools are yet another way we are using to acquire a collective wisdom on how to put a stop to coronary heart disease, heart attack, and perverse "let's make money with heart procedures" hospital solutions.

One of the aspects that helps make this work is the sharing of data. So far, the people who have begun to enter their data have all made their information "public." It's not truly "public," but viewable only by other Track Your Plaque Members. Also, Members can, in effect, anonymize their data simply by using a nickname, e.g., heartprotection or hearthawk.

The data tracking tools are in beta-test version, so there are bound to be a few glitches. But we're eager to hear from our Members' experiences on how to improve these tools. Report any problems or make your suggestions on the Track Your Plaque Member Forum--Technical Support.

Yet another reason to avoid fructose

Have you seen the Corn Refiners Association commercial campaigns to educate the American public on the safety of fructose? If you haven't, you can view these interesting specimens on You Tube:

"Get the facts--You're in for a sweet surprise: Fructose is safe in moderation!"

Two Moms

Two lovers


Beyond the fact that fructose stimulates liver production of glycerol, which thereby increases liver VLDL production and raises blood levels of triglycerides; likely stimulates appetite; increases cholesterol levels; fructose has also been clearly implicated in increasing blood levels of uric acid.

Uric acid is the substance that, in some people, precipitates in joints and causes gout, the painful inflammatory arthritis that has been increasing in prevalence over the last four decades since the introduction of fructose in 1967. While blood levels of uric acid in the early part of the 20th century averaged 3.5 mg/dl, more recent population assessments have averaged 6.0 mg/dl or higher. (Non-human mammals who don't eat processed foods, drink fruit drinks or beer, and don't eat candy have uric acid levels of <2.0 mg/dl.)

Uric acid is looking like it may prove to be an important risk factor for coronary disease and atherosclerotic plaque. It is no news that people with higher blood levels of uric acid are more likely to experience adverse cardiovascular events like heart attack. People with features of the metabolic syndrome also have higher uric acid blood levels; the more characteristics they have, the higher the uric acid level. However, the prevailing view has been that uric acid is simply an accompaniment of these processes, but not causal.

However, more recent observations suggest that increased levels of uric acid may instead be a cause of metabolic syndrome and high blood pressure.

Increased blood levels of uric acid have been shown to:

--Increase blood pressure
--Induce kidney damage (even in the absence of uric acid kidney stones)
--Antagonize insulin responses

A diagnosis of gout is not required to experience all of the adverse phenomena associated with uric acid. (For not entirely clear reasons, some people, perhaps based on pH or other factors, are more prone to trigger crystallization of uric acid in joints, similar to the phenomena of sugar crystallization when making rock candy.)

Which brings us back to fructose, a sweetener that clearly substantially increases uric acid levels. I suppose that the mothers and lovers in the Corn Refiners' commercials are right to a degree: Our kids will survive, as will you and I, despite increases in triglycerides, enhanced diabetic tendencies, amplified appetites, and increased uric acid due to fructose in our diet. We will also likely survive despite being 100 lbs overweight, partly due to the effects of fructose.

But if long-term health is your desire for you and your family, fructose has no role whatsoever to play.

Interestingly, the obviously expensive and slick ad campaigns from the Corn Refiners' videos have triggered some helpful video counterarguments:

High-fructose corn syrup
Conspiracy for Fat America
High-fructose corn syrup truth


A full discussion of uric acid, the scientific data behind uric acid as a coronary risk factor, and the nutritional means to reduce uric acid will be the topic of a thorough discussion in an upcoming Special Report on the Track Your Plaque website.

Free the Animal

Richard Nikoley from the Free the Animal Blog contributes this informative comment:



'Bout 18 months ago, I was at 230 (5'10) and looked awful. I was on Omeprezole for years for gastric reflux, a variety of prescription meds since early 20s for seasonal sinus allergies, culminating finally in the daily, year round squirts of Flonase-esque sprays (the best for control without noticeable side-effects), and finally, Levothroid for about the last 7 years or so, as I had elevated TSH (around 9ish).

My BP was regularly 145-160 / 95-110.

I decided to get busy. I modified diet somewhat, cutting lots of junk carbs, and began working out -- brief, intense, heavy twice per week. BP began coming down immediately, such that within only a couple of weeks I was borderline rather than full blown high. Then after about six months, a year ago, I went to full blown low-carb, high fat, cutting out all grains, sugar, veg oils, etc, and replacing with animal fats, coconut, olive oil. You know the drill. Then, first of the year I felt great and simply stopped all meds, including the thyroid. I also began intermittent fasting, twice per week, and for a twist, I always do my weight lifting in some degree of fast, even as much as 30 hours.

That's when the weight really started pouring off. Take a look:

http://www.freetheanimal.com/root/2008/09/periodic-photo-progress-update.html

http://www.freetheanimal.com/root/2008/08/faceoff.html

In July I figured it's about time for a physical. Here's the lipid panel, demonstrating am HDL of 106 and Try of 47, great ratios all around:

http://www.freetheanimal.com/root/2008/07/lipid-pannel.html

However, my TSH was even higher -- 16ish. It seems odd that I was able to lose 40-50 pounds of fat (10-15 pounds of lean gain for a 30 pound net loss at that time -- now an additional 10 pounds net loss).

One disclosure is that I was drinking too much, almost daily, and quite a bit (gotta save some vices...). Anyway, I'm at the point now where I want to drill down. I know I need to see an endocrinologist and have T3 and T4 looked at, but in advance, I wanted to see if the recent changes I've made could make a difference:

1. Stopped all alcohol.
2. Stopped most dairy, except ghee and heavy cream, and cheese is now used as a "spice," i.e., tiny quantities -- no more milk.
3. 6,000 IU Vit D per day.
4. 3 grams salmon oil, 2 grams cod liver oil.
5. Vit K2 Menatetrenone (MK-4) -- side story: getting off grains reversed gum disease for which I have had two surgeries, then supplementing the K2 DISSOLVED calculus on my teeth within days -- hygienist and dentist are dumbfounded. Stephan (Whole Health Source), who comments here, has an amazing series on K2.



If you view his photos, you'll appreciate just how far he has come.

Overall, Richard's program is wonderful and his pictures clearly display his success. However, Richard, thyroid function is indeed a problem, a problem that needs to be fixed ASAP. Remember, low thyroid function used to be diagnosed at autopsy at which time the coronary arteries and other arteries of the body were found to be packed solid with atherosclerotic plaque, even in young people.

I'd recommend:

1) Consider 200 mcg Iodine per day from kelp if you do not use iodized salt.

2) Seeing your doctor right away for thyroid replacement, hopefully with consideration of your T3 status.

3) A heart scan--Not to lead to procedures, but something for you to track over time as your program improves and thyroid function is restored.

Beyond this, keep up the great work. Great blog, too!

Low Thyroid and Plaque

Having now tested the thyroid status of several hundred patients over the last few months, I have come to appreciate:

1) That thyroid dysfunction is rampant, affecting at least 25% of everyone I see.
2) It is an enormously effective means to reduce cardiovascular risk.


I'm not talking about flagrant low thyroid dysfunction, the sort that triggers weight gain of 30 lbs, gallons of water retention, baggy eyes, sleeping 14 hours a day. I'm talking about the opposite extreme: the earliest, subtle, and often asymptomatic degrees of thyroid dysfunction that raises LDL cholesterol, lipoprotein(a) (Lp(a), a huge effect!), and adds to coronary plaque growth.

Correcting the subtle levels of low thyroid:

1) Makes LDL reduction much easier

2) Facilitates weight loss

3) Reduces Lp(a)--best with inclusion of the T3 fraction of thyroid hormone.

Recall that, 100 years ago, the heart implications of low thyroid weren't appreciated until autopsy, when the unfortunate victim would be found to have coronary arteries packed solid with atherosclerotic plaque. It takes years of low thyroid function to do this. I advise you to not wait until you get to this point or anywhere near it.

I find it fascinating that many of the most potent strategies we are now employing in the Track Your Plaque process are hormonal: thyroid hormones, T3 and T4; vitamin D (the hormone cholecalciferol); testosterone; progesterone; DHEA, pregnenolone. Omega-3 fatty acids, while not hormones themselves, exert many of their beneficial effects via the eicosanoid hormone pathway. Elimination of wheat and cornstarch exert their benefits via a reduction in the hormone insulin's wide fluctuations.

We haven't yet had sufficient time to gauge an effect on coronary plaque and heart scan scores. In other words, will perfect thyroid function increase our success rate in stopping or reversing coronary plaque? I don't know for sure, but I predict that it will. In fact, I believe that we are filling a large "hole" in the program by adding this new aspect.
Blame the niacin

Blame the niacin

Despite the fact that niacin is:

1) A vitamin--vitamin B3

2) One of the oldest cholesterol-reducing agents around with a long-standing track record of effectiveness and safety

3) Available as a prescription drug as well as a variety of "nutritional supplements"

most physicians remains shockingly unaware of its benefits, effects, and side-effects. Most, in fact, are either ignorant or frightened of advising their patients on niacin use. As a result, I commonly have to tell my patients to resume the niacin that their primary care physician has (wrongly) stopped because of itchy feet, grumpiness, groin rash, urinary tract infections, nightmares, diarrhea, hair loss, runny nose, etc. All of these are REAL reasons doctors have advised patients to stop niacin (though none were actually due to niacin).

Is niacin really that troublesome? No, it's not. In fact, if used properly, it's among the most effective and safe tools available for correction of low HDL, small LDL and other triglyceride-containing lipoproteins, lipoprotein(a), and dramatic reduction of heart attack risk. If added to a statin agent, the heart attack risk reduction can approach 90%.

Statins are just too easy for doctors to prescribe. Niacin, on the other hand, requires a good 15-20 minutes to describe how to use it. It could generate an occasional phone call from a patient who struggles with the annoying but largely harmless and temporary "hot-flush" feeling, a lot like a hot blush. Given a choice, most doctors would simply choose not to be bothered. For this reason, I'll commonly see many, many people with uncorrected low HDLs and other patterns.

Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

Here are the steps we advise that really make taking niacin easy and tolerable:

1) Take with dinner.

2) Take with 2 extra glasses of water. If you experience the hot-flush later on, drink an additional 2 8-12 oz glasses of water i.e., a total of 16-24 oz). Extra hydration is extremely effective for blocking the hot-flush.

3) Take a 325 mg, uncoated aspirin. This is only necessary in the beginning or with any increase in dose, rarely chronically for any length of time.


This is not to say that there aren't occasional people who are truly and genuinely intolerant to niacin. It does happen. But those people are a small minority, less than 5% of people in my experience. Niacin is far more effective and safe than most physicians would have you believe.

Comments (7) -

  • madcook

    10/31/2006 6:12:00 AM |

    I've taken prescription Niaspan for over an year and a half.  Several times I've had an unintended "untoward" reaction, more than a blush, more than a flush... more like a niacin storm!  Each time I've learned something new, however.  Yes, hydration is very important.  There are certain foods and drugs which apparently dam up the same metabolic pathway as niacin, and can cause a pretty nasty reaction.  Among these, at least for me, are certain long acting antibiotics (Zithromax), spicy chai tea, pepperoni (not supposed to go there anyway!) and very spicy foods, if taken near the time of Niaspan dosing.  I was advised by my Dr. that Benadryl syrup would help to shorten the duration of the "storm".  Mostly it's a case of dietary management and timing of dosage.  The good done by niacin certainly still outweighs the occasional bad side effects!

  • Jim

    3/14/2008 4:03:00 PM |

    Another comment about niacin from this long-time niacin user, maybe folks will find it useful...
    Dr. Davis's advice to hydrate heavily to prevent/reduce flushing is, alas, not completely effective. One can easily prove this for oneself. The next time you experience a big flush, consume as much water as you are able, and see if the flush quickly resides..does it?  No. Hydration is certainly great advice, I'm not knocking it, but as a flush reduction strategy, it isn't enough. One commentor here mentioned quercetin.  It seems some recent research on certain flavonoids (quercetin, luteolin) have produced good results,better than aspirin, which was mentioned in this thread.  One needs to experiment and see if supplements such as these do help, taken maybe 30-45 minutes before the niacin dose. I have some other comments on niacin strategies I've hardly seen mentioned anywhere, but I'll wait until (1) I see my posts are approved (I'm new here), and (2) that people are interested. Let's see if there is any feedback. Regards, Jim

  • mill

    6/27/2008 5:43:00 PM |

    I've been taking niacin  2 times daily for 6 months and dropped my cholestral from 240 to 162.  Can I go back to once daily?

  • Anonymous

    12/30/2008 10:15:00 PM |

    I have seen some research papers that report that NIACIN, Nicotinamide and/or SAMe ( maybe also other methyl donors such as TMG ) can cause Parkinson's disease. I wonder if niacin can be converted to Nicotinamide in the body. Please see their abstracts and URLs below. Thank you.



    Niacin Metabolism and Parkinson’s Disease

    Tetsuhito FUKUSHIMA1)
    1) Department of Hygiene & Preventive Medicine, Fukushima Medical University School of Medicine
    Abstract
    Epidemiological surveys suggest an important role for niacin in the causes of Parkinson’s disease, in that niacin deficiency, the nutritional condition that causes pellagra, appears to protect against Parkinson’s disease. Absorbed niacin is used in the synthesis of nicotinamide adenine dinucleotide (NAD) in the body, and in the metabolic process NAD releases nicotinamide by poly(ADP-ribosyl)ation, the activation of which has been reported to mediate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease. Recently nicotinamide N-methyltransferase (EC2.1.1.1) activity has been discovered in the human brain, and the released nicotinamide may be methylated to 1-methylnicotinamide (MNA), via this enzyme, in the brain. A deficiency in mitochondrial NADH:ubiquinone oxidoreductase (complex I) activity is believed to be a critical factor in the development of Parkinson’s disease. MNA has been found to destroy several subunits of cerebral complex I, leading to the suggestion that MNA is concerned in the pathogenesis of Parkinson’s disease. Based on these findings, it is hypothesized that niacin is a causal substance in the development of Parkinson’s disease through the following processes: NAD produced from niacin releases nicotinamide via poly(ADP-ribosyl)ation, activated by the hydroxyl radical. Released excess nicotinamide is methylated to MNA in the cytoplasm, and superoxides formed by MNA via complex I destroy complex I subunits directly, or indirectly via mitochondrial DNA damage. Hereditary or environmental factors may cause acceleration of this cycle, resulting in neuronal death.

    Key words:
    nicotinamide N-methyltransferase, 1-methylnicotinamide, poly(ADP-ribosyl)ation, mitochondria, complex I

    Pasted from http://www.jstage.jst.go.jp/article/ehpm/10/1/10_3/_article


    Parkinson's disease: the first common neurological disease due to auto-intoxication?
    A.C. Williams1, L.S. Cartwright2 and D.B. Ramsden2
    From the Divisions of 1Neurosciences and 2Medical Sciences, University of Birmingham, Birmingham, UK
     
    Parkinson's disease may be a disease of autointoxication. N-methylated pyridines (e.g. MPP+) are well-established dopaminergic toxins, and the xenobiotic enzyme nicotinamide N-methyltransferase (NNMT) can convert pyridines such as 4-phenylpyridine into MPP+, using S-adenosyl methionine (SAM) as the methyl donor. NNMT has recently been shown to be present in the human brain, a necessity for neurotoxicity, because charged compounds cannot cross the blood-brain barrier. Moreover, it is present in increased concentration in parkinsonian brain. This increase may be part genetic predisposition, and part induction, by excessive exposure to its substrates (particularly nicotinamide) or stress. Elevated enzymic activity would increase MPP+-like compounds such as N-methyl nicotinamide at the same time as decreasing intraneuronal nicotinamide, a neuroprotectant at several levels, creating multiple hits, because Complex 1 would be poisoned and be starved of its major substrate NADH. Developing xenobiotic enzyme inhibitors of NNMT for individuals, or dietary modification for the whole population, could be an important change in thinking on primary and secondary prevention.


    Pasted from http://qjmed.oxfordjournals.org/cgi/content/full/98/3/215

    see also
    http://www.springerlink.com/content/d5wurtwylvpcy04q/


    But,on the contrary,the paper below seems to suggest that niacin protects from Parkinson's.

    Title: Does diet protect against Parkinson's disease? Part 4 – vitamins and minerals
    Author(s): Isabella Brown
    Journal: Nutrition & Food Science
    ISSN: 0034-6659
    Year: 2004 Volume: 34 Issue: 5 Page: 198 - 203
    DOI: 10.1108/00346650410560343
    Publisher: Emerald Group Publishing Limited
    Abstract: This paper is the fourth in a series on Parkinson's disease and diet and investigates the role which antioxidant vitamins A and C, niacin and selenium may have on the incidence of the disease. Oxidative stress is believed to be a key factor in the development of PD and all of these have a role in preventing oxidative stress mediated cell damage. Dietary information was obtained via questionnaires. Vitamin C was found to reduce the risk of PD by 40 per cent in one study, although this was not supported by other studies. Niacin was associated with an at least 70 per cent reduced risk of PD incidence in a number of studies. No evidence was found to support a role for vitamin A or selenium. There is a need for further research to support or disprove the roles of these antioxidant vitamins within the aetiology of PD.
    Keywords: Diet, Diseases, Lifestyles, Vitamins
    Article Type: Research paper
    Article URL: http://www.emeraldinsight.com/10.1108/00346650410560343

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