Are there any alternatives to niacin?

10. September 2006 William Davis (0)
In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.
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If you need a reason to quit smoking...

If you need a reason to quit smoking...

26. April 2006 William Davis (0)
If you've read Track Your Plaque, you already know my feelings about smoking and coronary plaque. Smoke, and you will lose the battle for control over coronary plaque growth--it will grow and grow until catastrophe strikes.

Nonetheless, this is not sufficiently motivating for some people.

If you need more motivation to quit smoking, just take a look at your heart scan sometime, accompanied by either one of the doctors or technicians at the scan center you choose. After you've had an opportunity to look at your coronary arteries, take a look at the lungs. The heart is in the middle and the lungs are the two large black areas on either side of the heart. (They're not really black; that's just the way the images are color-coded.)

Smokers will see large cavities in their lungs--literally, half-inch to one-inch wide holes that contain only air. Many of them. These represent remnants of lung tissue, digested away and now useless from the damage incurred through smoking.

Non-smokers should see uniform lung tissue without such cavities.

What surprised me early on in my heart scan experience was how little smoking exposure was required to generate these cavities. A 40-year old, for instance, who smoked a half-pack per day for 10 years would have them. Heavier smokers, of course, showed far more extensive cavities.

Officially, these cavities are called "emphysematous blebs", meaning the scars of the lung disease, emphysema.

When I've pointed out these cavities or emphysematous blebs to patients, 9 out of 10 times they immediately become non-smokers. Commonly, they'd exclaim, "I had no idea I was really damaging my lungs!" Most admitted that they were awaiting some bona fide evidence that they were truly doing some harm to their bodies. Well, that's it.

Give it a try if you're struggling.
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Yet another reason to avoid fructose

Yet another reason to avoid fructose

6. December 2008 William Davis (5)
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.
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Comments (5) -

  • Kevin

    12/12/2008 8:02:00 PM |

    There was an article this week in USA Today about new research pertaining to high fructose corn syrup (independent of your uric acid argument). Check it out here: http://www.usatoday.com/news/health/2008-12-08-fructose-corn-syrup_N.htm

    -Kevin on behalf of the Corn Refiners Association

  • BenignaMarko

    12/18/2008 5:28:00 PM |

    This all sounds doable.  It does seem that fructose is causing such health problems that the FDA should make sure it is removed from products.  We all know that we consume too much everything, so, can't they make the stuff without the fructose?  There is so much to worry about in recent years, we might as well not eat.
    Benigna Marko

  • Anonymous

    1/4/2009 10:36:00 PM |

    I don't deny the research posted in this post.  However, things are not as simple as they seem.

    I have done quite a lot of research on Multiple Sclerosis, and high levels of uric acid are actually implicated in LOWER levels of MS.  Uric acid actually can work as an antioxidant in the body; gout and MS are almost mutually exclusive.  You will almost never see someone who has gout having MS, and vice versa.

    In fact, increasing uric acid in MS patients has been shown to DECREASE RELAPSE RATES (see abstract below.)

    So, things are not as simple as they appear.  

    Just thought I'd post this information.

    -gb

    FROM MEDLINE


    5: Vojnosanit Pregl. 2006 Oct;63(10):879-82.Links
        Therapeutic value of serum uric acid levels increasing in the treatment of multiple sclerosis.
        Toncev G.

        Clinical Center Kragujevac, Center of Neurology, Kragujevac, Srbija.

        BACKGROUND/AIM: Uric acid was successfully used in both, prevention and treatment of the animal model of multiple sclerosis (MS). Recently it has been shown that inosine, a ribosylated precursor of uric acid, might be used to elevate serum uric acid levels in MS patients. The aim of this study was to evaluate the safety and efficacy of oral inosine as a single drug treatment in patients with MS. METHOD: We administered inosine orally to 32 MS patients from 2001-2004 year at doses from 1-2 g daily (given twice) depending on the pretreatment serum uric acid levels. The mean follow-up interval was 37.69+/-6.55 months. The other 32 MS patients, without any treatment except for a relapse period (matched by age, sex, duration of disease and functional disability), were used as controls. The follow-up interval of these patients was 36.39 +/- 2.68 months. The neurological disability was evaluated by the Expanded Disability Status Scale score (EDSS). RESULTS: During the observed period the treated MS patients were found to have the lower relapses rate than the non-treated MS patients (Chi-square test, p = 0.001). None of the patients have showed any adverse effect of inosine treatment. The non-treated MS patients were found to have a higher increasing in the mean EDSS score than the treated ones (two-way ANOVA-repeated measures/factor times, p = 0.025). CONCLUSION: Our results suggested that the treatment approaches based on the elevation of serum uric acid levels might prove beneficial for some MS patients


    1: Eur J Neurol. 2008 Apr;15(4):394-7. Epub 2008 Feb 26.Click here to read Links
        Variation of serum uric acid levels in multiple sclerosis during relapses and immunomodulatory treatment.
        Guerrero AL, Martín-Polo J, Laherrán E, Gutiérrez F, Iglesias F, Tejero MA, Rodríguez-Gallego M, Alcázar C.

        Neurology Unit, Hospital Río Carrión, Palencia, Spain. aguerrero@hcuv.sacyl.es

        Uric acid (UA), a product of purine metabolism, may be an antioxidant, perhaps acting as a scavenger of peroxynitrite. Patients with gout have a reduced incidence of multiple sclerosis (MS). A number of studies found that patients with MS have low serum levels of UA, although it has not been established whether this represents a primary deficit or a secondary effect. UA has also been proposed as a marker of disease activity and response to immunosuppressive or immunomodulatory treatment. We retrospectively reviewed 83 relapsing-remitting or secondary progressive MS patients (64 females and 19 males) followed in our Neurology Unit. We collected data concerning demographic variables as age and sex, and clinical variables as age of onset, clinical type, disease duration, EDSS score and total number of relapses. We considered UA levels in three different situations: during a relapse, during remission period and during remission period under immunomodulatory treatment [Interferon Beta 1a i.m. (Avonex; Biogen Idec Inc., Cambridge, MA, USA), Interferon Beta 1a s.c. (Rebif; Serono Europe Limited, London, UK), Interferon Beta 1b (Betaferon; Bayer Schering Pharma AG, Berlin, Germany) or Glatiramer Acetate (Copaxone; TEVA Neuroscience LLC, Kansas City, MO, USA)]. A Wilcoxon matched pairs test was carried out to determine differences between groups. A P-value less than 0.05 was considered statistically significant. In 33 patients, we were able to compare at least one UA value obtained during a relapse with at least one when remission without treatment. Mean serum UA levels were significantly lower when measured during a relapse (r: 0.39, P: 0.024). In 27 cases, we compared at least one remission value without treatment with at least one obtained during remission and immunomodulatory treatment. Mean serum UA levels significantly increased when determined during Interferon Beta or Glatiramer Acetate therapy (r: 0.84, P < 0.001). Although we do not know exactly whether and how UA is involved in MS pathogenesis, our data suggest that UA might reflect disease activity or treatment response in MS.

  • karl

    2/28/2009 3:56:00 AM |

    I read that Fructose is 10 times more reactive than glucose in forming AGE - Advanced Glycogen End-products - the process thought to start CAD.

    I avoid all sugar - but wonder if the extra 5-10% might make a difference.

  • Free Teleconferencing

    2/22/2011 11:49:58 AM |

    Very... Nicee... Blog.. I really appreciate it... Thanks..Smile

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