Thank you, Crestor

20. March 2009 William Davis (9)
I'm sure everyone by now has seen the Crestor ads run by drugmaker, AstraZeneca. TV ads, magazine ads, and the Crestor website all echoing the same message:

"While I was busy building my life, something else was busy building in my arteries: dangerous plaque."

While previous drug trials with Mevacor, Pravachol, Zocor, and Lipitor have focused mostly on examining whether the drugs reduced incidence of cardiovascular events, Crestor studies have also focused on effects on atherosclerotic plaque volume. The best example is the ASTEROID trial that demonstrated approximately 7% reduction in plaque volume by intracoronary ultrasound.

So the AstraZeneca decision makers took the leap from cholesterol reduction to plaque reduction.

I'm sure this switch wasn't taken lightly, but was the topic of discussion at many meetings before the decision to make plaque reduction the focus of hundreds of millions of dollars of advertising. After all, billions of dollars are at stake in this bloated statin market.

Ordinarily, I couldn't care less about how the drug manufacturers conduct their advertising campaigns. But this one I paid attention to because the Crestor ads are helping fuel a new way of thinking about coronary heart disease: It's not about the cholesterol; it's about the atherosclerotic plaque that accumulates in arteries.

It's not cholesterol that grows, limits coronary blood flow, and causes angina. It's not cholesterol that "ruptures" its internal contents to the surface within the interior of the blood vessel and causes blood clot and heart attack. It's not cholesterol that fragments from the carotid arteries and showers debris to the brain, causing stroke. It's all plaque.

I took the same leap years ago, though not backed by hundreds of millions of dollars of marketing money. When I first called my book Track Your Plaque, some of the feedback I got from editors included comments like "I thought this was a book about teeth!" Even now, the word "plaque" in the book title and website is responsible for confusion.

But AstraZeneca is helping me clear up the confusion. As the word plaque gains hold in public consciousness, it will become increasingly clear that cholesterol reduction is not what we're after. We are looking for reduction of plaque.

If you are trying to develop an effective means to reduce or reverse coronary heart disease, then there are two simple equations to keep in mind:


Plaque = coronary heart disease

Cholesterol ? coronary heart disease


Plaque is the disease, cholesterol is not. Cholesterol is simply a crude risk for plaque.

While I'm no friend to the drug industry nor to AstraZeneca, some good will come of their efforts.
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Comments (9) -

  • Greg

    3/20/2009 6:12:00 PM |

    This is all so true. What makes me even more mad is my Dad is on some cholesterol lowering drug and no matter how much evidence I show against it he does not believe that his doctor would not do what is best for him. Makes me sick when I think about it.

  • Judy Graves

    3/21/2009 3:43:00 AM |

    I am currently in a battle with my "preventative" cardiologist.  she just handed me a bunch of Crestor due to a very high Lp(a) and family history of heart disease.  I have gone round and round with her about statins and she was willing to go the Niacin route first.  I was convinced that would work but something very strange occurred.  I don't mind the Niacin flush at all and I did take with food, aspirin, the whole 9 yards.  After being on the Niaspan for 12 days, I suddenly broke out into horrible hives all over my body and now 3 weeks later I still have some lingering rash/hives on my arms.  My diet and exercise program couldn't be better - I walk 6 miles a day, yoga 3 times a week, eat whole foods only, drink lots of water and I am just not sure what to do next.  My Lp(a) number is 135 and my total cholesterol is 267 with a not so good "ratio".  If anybody has any suggestions or comments I would love to hear them!

  • David

    3/21/2009 7:18:00 PM |

    Judy, make sure you take a close look at the hormones (estrogen, DHEA, thyroid, etc.), as these can influence Lp(a) to a pretty large degree.

    High dose EPA/DHA from fish oil is also really important. Consider up to ~6,000 mg EPA + DHA daily.

    Consume raw nuts and seeds. Almonds and ground flaxseed are great, and can help in dropping Lp(a).

    L-carnitine can help in lowering Lp(a), at least by a little bit.

    Not sure what you're including when you say your diet is made up of "whole foods." If this refers to things like "whole wheat," then that's problematic. Based on the research I've seen, those of us with Lp(a) (and yes, I am one of them too) are quite a bit more sensitive to the carbs. Eat carbs, and your Lp(a) goes up. Eat lower carbs, higher fat (particularly saturated), and your Lp(a) goes down. I would be loving on the coconut oil if I were you (and that's exactly what I do).

    As for exercise, I would start changing it up. That's an awful lot of walking, and it's not going to create the hormonal response that you need. The real benefit is in the high intensity stuff. Short, vigorous sprints, squats, that sort of thing. Check out www.crossfit.com for some idea of what I'm talking about.

  • Adam Wilk

    3/22/2009 3:30:00 PM |

    Judy,
    I second what David says above--it sounds like good, solid advice.
    I would add 3 things to the supplement category--Vitamin C (min 6000mgs/day) L-Lysine (min 6000mgs/day) and NAC, (min 1200mgs/day)
    The Vitamin C and L-Lysine combination is I'm sure you know, the Pauling-Rath formula--it's been around a long time, many swear by it, but it's never been clinically double-blind tested.  The NAC, I recently learned, is possibly the most powerful natural Lp(a) inhibitor out there, for now, anyway.  I was so swayed by what I read about it, I purchased a couple of bottles of it to add to Pauling-Rath, since I, too, am sometimes irked by the Niacin flushes I begin experiencing as I get closer to the 500mg dose--and this is after weeks of slowly titrating the dose so that I may avoid that uncomfortable event.
    Judy, also keep in mind, I've always read that 1)It's better for women to have higher cholesterol levels and 2) up until a few years ago, a cholesterol level of over 300 was considered high.  Now that '200' is the new '300', there seems to be quite a market for new prescriptions, nu?
    Adam

  • David

    3/22/2009 7:49:00 PM |

    The Pauling/Rath therapy is indeed intriguing. Before I discovered Dr. Davis and the TYP program, I thought that the Pauling therapy was the answer to heart disease.

    I now believe and am convinced that there's more to it than that, and I think Dr. Davis has one of the best, most comprehensive programs for heart disease out there.

    However, this is not really a criticism, and I remain convinced that there is value to the Pauling/Rath therapy. It makes so much sense, at least theoretically in terms of reducing Lp(a), and it has quite a bit of anecdotal evidence behind it (not to mention the research carried out by Rath, complete with CT scans). It seems like the experience of doctors using this therapy with their patients varies quite a bit, though. Some doctors swear by it, while others say it just doesn't work. It's only for this reason that I usually don't bring it up until I've brought other ideas to the front that I know are very effective.

    I've got my dad on the Pauling therapy, along with these other things (basic TYP stuff), and we'll be getting his Lp(a) rechecked soon. Should be interesting to see how much it has come down, though I won't know which factor (niacin, diet, carnitine, fish oil, etc.) is creating the most change. I just decided to hit it with everything we've got.

    Oh, and it's the same with the NAC. There are pockets of stunning success, but there's also worry about long term safety and the development of pulmonary hypertension. Is that a real danger? I don't know. I would guess not, personally, but at the same time I'd rather mention the "tried and true" methods first that have the most overall benefit.

    I'm glad the Pauling therapy was brought up, here. I think it definitely should be looked into more, and people need to be aware of it as an option that many are having success with.

    David

  • xenolith_pm

    3/31/2009 4:00:00 PM |

    This may be of interest to those who may want to reduce the risk of venous thromboembolism (VTE) with a statin (Crestor):

    http://www.usatoday.com/news/health/2009-03-29-statin-clots_N.htm

    Statin Crestor lowers risk of deep-vein clots

    "ORLANDO — (3/30/09) Researchers have shown for the first time that a potent cholesterol-lowering drug, Crestor, reduces the risk of deep vein thrombosis, or "economy-class syndrome," caused by potentially lethal blood clots that start in the veins and migrate to the lungs, sometimes after long flights.

    The evidence, out today, is the latest to emerge from the landmark JUPITER trial, which showed that statin treatments can cut in half the risk of heart attacks and strokes even in people with normal cholesterol levels."

    No other medicine has been shown to safely prevent these blood clots, which occur in at least 350,000 people a year and kill as many as 100,000 of them. The standard remedy once thrombosis has occurred is the drug warfarin, which, unlike statins, can promote bleeding.

    Statins are "a remarkably benign therapy," says senior investigator Paul Ridker of Brigham and Women's Hospital in Boston. "The thing that's really exciting is that there is no bleeding risk."

    Other studies have hinted that statins also reduce clot formation, but their power to prevent deep vein thrombosis was unknown. Ridker and his co-workers decided to use JUPITER to test the theory. A total of 17,802 people were randomly assigned to treatment and placebo groups. They were followed for nearly two years, on average.

    Deep vein thrombosis occurred in 34 patients taking Crestor and 60 people who were taking placebos, indicating that treatment reduced the risk of clots by 43%. Ridker says he believes that other statins would also reduce the risk.


    What I take from this;

    The dose of Crestor in JUPITER was 20mg.  Paul Ridker said that this is a remarkably benign therapy?  I think not, given Dr. Davis' descriptions of intolerable side effects that will inevitably occur to the majority of people at this dosage.  I've never used Crestor, but I have used 10mg Zocor and developed mild myopathy in my legs after only three weeks, so I'll take his word that I would be a poor candidate.

    I think the most interesting part of the press release is that JUPITER (like the other statin trials) in no way confirms what mechanism may be behind the reduced risk of VTE.  Could it be due to a lowering of vascular inflammation as indicated by a lower CRP?  That certainly makes sense.  It would be really great to get a definitive answer, since CRP can be effectively managed by other means than taking such a strong statin like Crestor.

    AstraZeneca's press release of CRESTOR® REDUCED RISK OF BLOOD CLOTS IN THE VEINS (3/29/09):

    http://www.prnewswire.com/mnr/astrazeneca/37394/

  • crestor

    5/9/2009 10:48:00 AM |

    AstraZeneca’s (AZN.L)(AZN.N) powerful cholesterol drug Crestor cut the risk of dangerous blood clots in the vein by 43 percent in a large study, researchers said on Sunday.

  • buy jeans

    11/2/2010 8:36:56 PM |

    After being on the Niaspan for 12 days, I suddenly broke out into horrible hives all over my body and now 3 weeks later I still have some lingering rash/hives on my arms.

  • Crestor

    11/16/2010 11:53:59 AM |

    Took it for a year or so, but now I need it again and my insurance wont pay for it and my other medicines are over $400.00 a month and they want $160.00 more for Crestor. We just can't do it.

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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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