Busting myths: In measuring cholesterol and heart health…Keep it simple.

Let’s talk about the newest cholesterol myth gone busted.

I can hardly write; I’m so giddy. That’s what happens to me when simplicity and obviousness triumphs over complicated testing that adds nothing to (or even clouds) the big picture.

Are you kidding me?

They come to my office with pages of data dissecting the particle sizes and sub-fractions of cholesterol–Apo this and that. Truth be told, I’ve never understood this data. These pages stream with nonsense. Get this: nuclear magnetic resonance spectroscopy determines the sizes and concentrations of cholesterol particles. (What?) LDL and HDL (and even VLDL) levels are broken down into component parts. Graphs are plotted, risk profiles drawn and money is charged. All this is done in the name of predicting heart events–let’s say for a VIP patient who carries 50 extra pounds, never exercises and can’t sleep because he’s worried about his business.

A few small studies have correlated certain particle sizes with cardiovascular risk. (I’m not saying which ones—because as you can guess it doesn’t matter.) More than studies though, this fad was fueled by the false notion—so ingrained in those drawn to complexity— that better health can be had with more testing and more therapy. This is wrong, and I am happy to tell you about the downfall of complex cholesterol particle analysis. As always, I’ll describe the details of the story and then the big picture.

The details on the downfall of cholesterol particle testing:  In this week’s issue of Circulation, researchers from the UK published an analysis of 5000 vascular events from the Heart Protection Study–a 20,000-patient, 5-year study of high-risk patients treated with either simvastatin or placebo/vitamins. The researchers studied how well regular cholesterol levels and said special analysis of cholesterol fractions (ApoB, Apo A1, and lipoprotein particles) predicted heart events. The results were clear: though each of the measures individually predicted events, the complicated analysis of particle sizes added no incremental value over just a simple cholesterol test.

An accompanying editorial by Dr. Ira Ockene, from the Univ. of Massachusetts, summed up the conclusion beautifully: (emphasis mine)

“…[We] need to recognize that our hunt for progressively finer discriminatory tools for risk assessment is a misplaced effort. The underlying assumption is that we have difficulty recognizing who is at risk. This is not the case. We know how to recognize those at risk for atherosclerotic disease. It used to be said that many myocardial infarctions (heart attacks) occur in people without abnormalities of traditional risk factors. This is a myth.”

Dr. Ockene goes on to cite multiple trials confirming the fact more 90% of heart events occur in people with at least one risk factor other than cholesterol levels. Though his vernacular is different from mine, his words capture my feelings well:

“Our greatest problem is delivering appropriate risk factor modification to those in whom the risk is obvious; it is useful to seek better discrimination of risk in those at the margins, but it is not where our greatest effort should be focused…

… A physician can, in quite a short interval of time, easily categorize a patient’s risk. Our greatest effort must be directed toward the overall reduction of cardiovascular risk: behavior change with regard to smoking, obesity, unhealthy diet, inadequate physical activity, and psychosocial factors such as stress and depression; greater attention to the health of our children and the facilitation of healthy behavior throughout the life course, prescription of appropriate medication for hyperlipidemia and hypertension with attendant emphasis on medication adherence; and systematic public health and societal strategies that support beneficial change. The tools we have available to define cardiovascular risk are quite adequate to the task; we now need to improve their utilization so as to further reduce the population burden of cardiovascular disease.”

Let me translate the Massachusetts’ language:

The big picture: With two eyes, a scale, a blood pressure cuff, a one-minute blood test for sugar and a three-minute conversation, a doctor can predict cardiac risk as well as a 100$ multi-page list of cholesterol particles. Attention can then focus on the three components of health: good movement, good food and good sleep.

Happy am I that the thesis of DrJohnM remains sound: Heart health can be measured and achieved simply. It’s not complicated.

My apologies to smart people who like their data more granular.

JMM

Comments

  1. says

    John – I hope you can become a family physician in your “after-life”. Your philosophy and perspective is so totally refreshing! (as well as being “spot-on”).

    This post about cholesterol fraction analysis supports what I’ve intuitively felt (and experientially witnessed) over the many years I taught family medicine residents. Your concluding “big picture” summary at the end of your post is not only a more meaningful assessor of cardiac risk – but far cheaper (and I believe much more reproducible) than any cholesterol fractioning could be (in my humble opinion). KEEP UP the great work on your blog!

  2. says

    But Dr. John, think of all those researchers, journal editors, “thought leaders”, drug reps and Big Pharma stakeholders who’ll be unhappy if you drill down the data in such a brilliantly common sense fashion!?

  3. Jay says

    It’s been a tough couple of years for the lipidologists, hasn’t it.

    Lately those pushing all this crap are starting to look like the Wizard of Oz at the end of the movie when he tells Dorothy and crew that there’s nothing interesting behind the curtain.

    Look at all that has fallen or come into question recently–Zetia, CTEP inhibitors, the notion of statins in primary prevention, the HDL hypothesis, the role of surrogate markers (such as carotid intimal ultrasound), safety of high dose statins, and now all those crazy Apo this and thats. Am I missing anything?

    I’m starting to believe that I’ve been the smart one sitting all of this out until the dust settles.

    Someday, it seems likely to me, everything but responsible statin use in appropriately risk stratified patients will likely fall to the wayside. Its’ gonna take a while, though. There are still a few more CTEP inhibitors and monoclonal antibodies on the horizon still waiting for the seemingly inevitable neutral or negative cardiovascular outcomes study.

    Clearly I do not have the lipid knowledge base to make these proclamations, which I’m sure would be insulting to the scientists. Nevertheless, the vibes seem pretty strong to me. It’s also easy to speculate how the “lipid-industrial complex” could make this stuff wind on forever given the financial stakes at work.

    Thanks for your clear headed take on on this.

    Jay

  4. says

    After reading this blog entry, all I can think about is my gleeful expression during lunch next time one of the “particle hawkers” comes to our office. I feel better knowing that one of our well-respected cardiologists feels the same way this lowly PCP does when presented with one of these cardiac risk “panels”. KISS is my motto and I think it serves the patient well (Keep It Simple Stupid). Thanks for clearing the air.