The Framingham Crap Shoot

The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians.

The Framingham system determines that:

· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary.

· 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice.

· The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment.


Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year.

The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year.

The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year.

These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.

The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not.

From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack.

For any specific individual (like you or me), it’s a crap shoot.

That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score.

Comments (2) -

  • katherine

    11/24/2008 3:31:00 PM |

    just came across this...thoughts?

    http://thegearjunkie.com/the-runners-heart

  • John

    11/29/2008 3:33:00 AM |

    Good article. One of the most common mistakes made by health conscious individuals is the idea that if study X says A is bad or good then one should adjust one's lifestyle accordingly.

    If only it were that simple. A statistical analysis of a group is applicable to that group, not necessarily the specific individuals within that group; let alone those outside the studied group. We cannot determine individual risk on the basis of such studies yet time and again these studies are mentioned as "evidence" that we must accept. Sadly, too many health promoters, who should know better, tend to make the same logical error.

    Very pleased to see that this error is highlighted here.

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Thank you, Crestor

Thank you, Crestor

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.

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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