Category Archives: Statin Drug Therapy

Are You Paying More For Rosuvastatin (Generic Crestor) Than Brand Name Crestor?

The skeptical cardiologist was shocked to hear from a patient last week that she would have to pay considerably more for generic rosuvastatin (GR) than Crestor, its brand name equivalent.

Crestor is the most potent statin we have at lowering LDL (bad) cholesterol, raising HDL (good) cholesterol, and  preventing strokes and heart attacks.  It is also the best tolerated statin in my experience; I use it frequently at low or intermittent dosages in patients who have developed muscle aches on other statins.

In comparison to atorvastatin (Lipitor, the most widely prescribed statin), Crestor is less likely to interact with other medications and (very important for a surprising number of my patients), you can consume grapefruit when taking it.

When a generic (rosuvastatin calcium) of Crestor became available last year I rejoiced, believing that the high cost of Crestor would now drop to the levels we have typically seen with other generic statins.

I have been giving Crestor sample packs like these to my patients for years. Alas, they will fade away. One downside to going generic.
I have been giving Crestor sample packs like these to my patients for years. Alas, they will fade away. One downside to going generic.

For example, when Lipitor (atorvastatin, the statin market leader for 20 years) went generic, patients no longer worried about its cost.

Initially it seemed GR was much more affordable for my patients than Crestor, however recently, I have had many of them report a rise in its cost.

Why Would The Generic Cost More Than Crestor?

The reasons for brand name versus generic pricing are many and complex, and they yield insight into the legal machinations that Big Pharma engages in to maintain high patient pharmaceutical costs.

This NY Times piece from July, 2016 reveals  how hard AstraZeneca fought to protect its exclusivity in selling Crestor and to prevent generics from entering the market. AstraZeneca’s last tactic involved a lawsuit claiming that their patent was protected by the orphan drug act. They lost and were heavily criticized:

“This case is not about the medical needs of a small population of pediatric patients with a rare disease,” the F.D.A. and Justice Department said in a brief filed in the lawsuit. “It is about AstraZeneca’s profit-driven desire to substantially extend its virtual monopoly on one of the world’s most popular medicines.”

There are other factors that slow the drop in generic prices. Consumer Reports, writing on the anticipated release of GR in May quoted an expert thusly:

“While some pharmacies drop the price as generics enter the market, others will hold it near the brand-name price as long as possible.” They get away with it, he says, because many customers who have health insurance pay a set co-pay regardless of the retail price. But those consumers who pay the entire cost of the drug themselves because they don’t have insurance or have a high deductible may not see the substantial savings that should come with generic availability.”

What an individual pays for drugs varies wildly depending on their insurance coverage. These costs are extremely hard for a physician to anticipate and rarely reflect the actual cost of drugs. Thus, in America, patients as consumers are often isolated from the true costs of pharmaceuticals to society.

Geo (he who was “on the fence” about taking a statin) asked me the following reasonable question about his GR prescription:

I did not pay anything for the 25 pills, however the paperwork states a cost of $220 if I had to buy this outside of a health insurance plan. Do you know if the health insurance company is being charged the $220, or do they negotiate a lower cost with the manufacturer?
I don’t have that answer, but would love to know it. This kind of information is hard to get at.
Send Me Your Observations On The Cost of Generic Rosuvastatin
I would like to get input from my patients and readers on their experience regarding the cost of GR to them and/or their insurance company.
I’d also appreciate input from those in the pharmaceutical or insurance portion of this equation (I know I have at least one patient who is in the pharmaceutical industry).
Finally, if any of you have experience with purchasing GR online from international pharmacies, please share it below. For example, this site claimed in May, 2016:
Ninety pills of generic rosuvastatin cost a whopping $795 at a Walgreens in Brooklyn, NY, but 90 pills of brand name Crestor is $45.65 at a low-cost international online pharmacy,
Specifically Yours,

Are You On The Fence About Taking A Statin Drug?

The father of the eternal fiancee’ of the skeptical cardiologist (FOEFOSC, let’s call him “Geo”) is a typical 61 year old white male. A year ago his primary care physician informed him that he needed to start taking a statin drug because his cholesterol was high. The note accompanying this recommendation also stated “work harder on diet and exercise to get LDL<130.”  No particulars on how to change his current diet and exercise program were provided.

Neither of Geo’s parents and none of his siblings have had heart problems at an early age and Geo is very active without any symptoms. His diet is reasonably free of processed food and added sugar, he is not overweight and his blood pressures are fine. Due to concern about side effects he had read about on the internet and because he doesn’t like taking medications , Geo balked at taking the recommended statin,

Reluctance to start a new and likely life-long drug is understandable especially when combined with a constant stream of internet-based bashing of statins.

My advice was sought and I suggested a few things that would be helpful in making a more informed decision:

-Calculate Geo’s 10 year risk of heart attack and stroke using the ACC ASCVD Risk estimator app.

-Assess for early or advanced build-up of atherosclerotic or fatty plaque in the carotid arteries (vascular ultrasound) and coronary arteries (coronary calcium scan).

As I’ve pointed out before (here), the vast majority of men over the age of 60 move into a 10 year risk category >7.5%, no matter how great their lifestyle is, and Geo was no exception with a risk of 8.4%. His total cholesterol was 249, LDL (bad) 154, HDL (good) 72 and triglycerides 116.

The vascular ultrasound showed below normal carotid thickness and no plaque and his coronary calcium score was 18,  putting him at the 63rd  percentile. This is slightly higher than average white men his age.

When Geo presented these findings to his PCP, he seemed unaware of the ASCVD risk estimator (recommended by AHA/ACC guidelines first published in 2013), which no longer suggests LDL levels as goals. His PCP also seemed miffed that he had gotten the coronary calcium scan. Geo felt like the PCP’s attitude was “shut up and do what I tell you.”

Geo’s PCP’s approach exemplifies a not-uncommon traditional doctor-patient relationship, but a better approach is shared decision-making (see here). Geo, like many patients, welcomes more information on the risks and benefits of any recommended treatment so that he can participate in deciding the best course of action.

I steer patients who want more complete information towards my  evidence-based blog posts on statins (see here for discussion on statin side effects and here for statin benefits beyond cholesterol lowering.)

By giving patients more information on the risks, side effects, and benefits of the statin drugs along with a better understanding of their overall risk of heart disease and stroke, we can hopefully move more patients “off the fence” and onto the most appropriate treatment.

Stay tuned to find out what The Skeptical Cardiologist Recommended for Geo.

Decisively Yours


For more discussion on the value of coronary artery calcification (CAC) and the value of statin in lower risk patients see this recent paper entitled “Refining Statin Prescribing in Lower-Risk Individuals: Informing Risk/Benefit Decisions”(PDF refining-statin-prescribing-in-lower-risk-individuals-informing-riskbenefit-decisions)

If you’d like to read the recently published recommendations of the US Preventive Services Task Force on statins for primary prevention of cardiovascular disease see here. Importantly this panel of unbiased experts concluded that statin therapy significantly reduced overall mortality and cardiovascular mortality. In addition, the review found no increased risk of diabetes overall with statin therapy. The only trial that identified an increased risk was using high intensity statin therapy (Crestor (rosuvastatin) >20 mg).

And,  since the internet is jammed with people who believe statins robbed them of their brain power, I would advise noting that the writers concluded  “These findings are consistent with those from a recent systematic review of randomized trials and observational studies that found no adverse associations of statins with incidence of Alzheimer disease, dementia, or decreased scores on tests of cognitive performance.”



Donald Trump Has Moderate Plaque Buildup In His Coronary Arteries and his Risk For A Cardiac Event Is Seven Times Hilary Clinton’s Risk

Donald Trump recently appeared on the Dr. Oz show and handed a letter to the celebrity medical charlatan and TV host, Mehmet Oz.

The letter was written by his personal physician , Dr. Harold Bornstein,  screen-shot-2016-10-04-at-3-21-11-pm
and summarized various  laboratory and test  results which led Bornstein to conclude  that Mr. Trump is in excellent health (Bornstein did not repeat his earlier, bizarre statement that “If elected, Mr. Trump, I can state unequivocally, will be the healthiest individual ever elected to the presidency.”)

From a cardiovascular standpoint the following sentence stood out:

“His calcium score in 2013 was 98.”

Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now.  I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain  patient’s risk of sudden death and heart attacks.

coronary calcium
Image from a patient with a large amount of calcium in the widowmaker or LAD coronary artery (LAD CA).

The CAC scan utilizes computed tomography (CT)  X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.

Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.

What Does Donald’s Trump’s Calcium Score Tell Us About His Risk Of A Major Cardiac Event?

We know that, on average, even if you take a statin drug (Trump is taking rosuvastatin or Crestor), the calcium score goes up at least 10% per year which means that 3 years after that 98 score we would predict Trump’s calcium score to be around 120.

Based on large, observational studies of asymptomatic patients, Calcium scores of 101 to 400 put a patient in the moderately high risk category for cardiovascular events.

When I read a calcium score of 101-400, I make the following statements (based on the most widely utilized reference from Rumberger

This patient has:

-Definite, at least moderate atherosclerotic plaque burden

-Non-obstructive CAD (coronary artery disease) highly likely, although obstructive disease possible

-Implications for cardiovascular risk: Moderately High

Patients in this category have a 7-fold risk of major  cardiac events (heart attack or death from coronary heart disease) compared to an individual with a zero calcium scorescreen-shot-2016-10-04-at-3-16-25-pm



Clinton versus Trump: Zero is Better

Since we know that Hillary Clinton recently had a calcium scan with a score of zero, we can estimate that Trump’s risk of having a heart attack or dying from a cardiac event is markedly  higher than Clinton’s.

Clinton, born October 26, 1947 is 68 years old and we can enter her calcium score into the MESA calcium calculator to see how she compares to other women her age. A  coronary calcium score of 6 is at the 50th percentile for this group.

Interestingly, Trump’s score of 98 at age 67 years was exactly at the 50th percentile. In other words half of all white men age 67 years are below 98 and half are above 98, creeping into the moderately high risk  category.

(This should not be surprising, I touched on the high estimated cardiovascular risk of all aging men in my post entitled “Should all men over age sixty take a statin drug?”)

So, based on his coronary calcium score from 2013, Donald Trump has a  moderate build up of atherosclerotic plaque in his coronary arteries and is at a seven-fold higher risk of a cardiac event compared to Hilary Clinton.

Let the law suits and tweets begin!

Electorally Yours,






Does Pravastatin Lower Your Risk of Diabetes?: The Joys of Continuing Education From Patients

One of the amazing perquisites of being a doctor is the opportunity to talk to a wide diversity of individuals with fascinating backgrounds and interests. I’ve always had some appreciation of this during my office interactions, but with age and ripening, I have come to relish and savor these conversations.

The skeptical cardiologist learns something from virtually every patient visit.  On a recent office day, I received patient pearls on topics ranging from Viking River cruises in Germany, to the method by which Express Scripts squeezes money from Walgreens and drug manufacturers, to certain novels of T. Coraghessan Boyle not centered on the maniacal vegetarian John Harvey Kellogg.

Not uncommonly, I’ll learn something about medicine or cardiology if I listen closely to my patients and keep an open mind.

I saw a 69 year old woman (we’ll call her Donna) the other day who had advanced plaque in her coronary arteries and with whom I had  initiated a discussion on the pros and cons of taking a statin drug to lower her risk of heart attack and stroke. This was not the first time we had talked about this topic; in previous visits she had shared with me her great fear of statin side effects and her desire to modify risk by dietary modification. On this visit, she came prepared with more research she had done on statins, and told me she was concerned about an increased  risk of diabetes with statin drugs.

I gave her my standard spiel:  statins, especially more potent ones like rosuvastatin and atorvastatin, appear to increase the risk of diabetes by 10-20%, however, this is offset by the benefits of statins, especially in someone with significant atherosclerosis, in reducing heart attack and stroke.

Donna then told me that she had read that pravastatin lowers the risk of diabetes. I hadn’t heard this (or more likely this slipped out of my ever-shrinking cerebral database) previously. Ten years ago, in the era before routine use of electronic health records (EHR), I would have had to just admit my ignorance and promise to look into that claim later (something that would not consistently happen due to time constraints and forgetfulness).  However, now I enter the patient exam room with my MacBook Air, primarily to access the patient’s EHR and look at old notes, cardiac tests etc.

Increasingly I also use the Mac to quickly look up information about a topic the patient has brought to my attention – either double checking what I believe to be true or researching claims I am unfamiliar with.

Often, the topic raised is the “snake oil du jour” (for example, is turmeric a cardiovascular panacea?), but in this case and many others, it is a relevant question about the nuances of disease or my proposed treatment.

A quick search (20 seconds) pulled up a 2009 meta-analysis of randomized trials of statins and the risk of diabetes. Sure enough, one of these trials (the West of Scotland Coronary Prevention Study) actually showed that patients treated with 40 mg of  pravastatin had a 30% lower risk of developing diabetes.  Four studies showed no effect of statins on risk of developing diabetes and only one, the JUPITER trial utilizing rosuvastatin (Crestor), showed a slight increase.

For some patients like Donna, a higher risk of diabetes may be a deal breaker for taking a life-saving medication. Although I can confidently tell her that the benefits outweigh the risks, if she has a specific fear of diabetes, perhaps related to a family member who had horrific complications of the disease, she could easily decline to take statins.

In Donna’s case, this new information about pravastatin, confirmed by the wonders of Google and a fast WiFi connection led to her giving statins (in the form of pravastatin) a chance.

I’ll remember this patient-triggered drop of wisdom for future discussions with patients whose  grave fear of diabetes makes them balk at taking statins.

Corasonically Yours,








west of scotland

Death Knell For Niacin For Lipids Sounded by FDA?

The skeptical cardiologist stopped writing new prescriptions for niacin extended release tablets in 2011. For any patient who was taking niacin, I recommended stopping it.

Because niacin had favorable effects on the cholesterol profile, physicians had been utilizing it for many years in high risk patients on statins who had low HDL  (good cholesterol) and/or high triglycerides.

The rationale was that, since high HDL was associated with lower risk of heart attacks, raising the HDL would lower that risk. Similarly, lowering the triglycerides would improve cardiovascular risks.

While niacin certainly improved the cholesterol profile, there was no good evidence that starting it in a patient already on statin would improve cardiovascular outcomes. The cholesterol profile is a surrogate endpoint: the actual treatment goal is reducing cardiovascular disease.

In 2011, the AIM-HIGH study proved there was no benefit to adding niacin to good statin therapy despite increasing HDL from 35 to 42 mg/dl, lowering triglycerides and lowering LDL. This and other studies showing no benefit of niacin therapy (and worrisome adverse effects) should have resulted in the total cessation of niacin prescriptions, especially  in patients on statins.

Unfortunately, old habits die hard amongst physicians, and the allure of raising HDL and lowering triglycerides with niacin persisted despite a lack of evidence of any benefit in lowering cardiovacular risk.

Yesterday, the FDA announced it was removing from the market two  drugs made by Abbvie, Advicor and Simcor, which are combinations of extended release niacin plus lovastatin or simvastatin, and removed its approved indication for niacin ER plus statin for lowering CHD risk stating:

“Based on the collective evidence from several large cardiovascular outcome trials (Refs. 1-3), the Agency has concluded that the totality of the scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events. Consistent with this conclusion, FDA has determined that the benefits of niacin ER tablets and fenofibric acid DR capsules for coadministration with statins no longer outweigh the risks, and the approvals for this indication should be withdrawn.”

This is good news for patients whose physicians were keeping them on the unproven brand name combination drugs, Advicor and Simcor.

There are still legitimate uses of niacin to prevent vitamin deficiencies but If you are still taking some form of niacin ER for the purpose of preventing heart disease with or without a statin I recommend presenting your doctor with the link to the FDA pronouncement above and having a good discussion with him about the rationale for staying on it.

The other drug mentioned in the announcement, fenofibric acid,  is far less often prescribed and is not available as a combination. It is the most effective drug we have for extremely high triglyceride levels over 500 mg/dl which can cause pancreatitis. I have a few patients on the generic fenofibric acid strictly for the purpose of lowering their dangerously high triglycerides but not for the indication of lowering their cardiovascular risk.

Nonsurrogateingly Yours



Doctor, My Cholesterol Levels Are Good. Why are You Starting a Statin?

I get this question frequently from patients.

It is a reasonable question. If statins are a treatment for abnormally high cholesterol levels why would we start them on a patient with normal or low levels.

ather_lowresThe answer is that we are not concerned with cholesterol levels. What we are concerned with is atherosclerotic cardiovascular disease (ASCVD) and its downstream consequences including heart attack and stroke.

Thus, the new guidelines recommend  calculating a patient’s 10 year risk of heart attack and stroke due to ASCVD ( see here for my discussion of smart phone app that makes this calculation) and if it is over 7.5% to consider starting a statin drug to reduce ASCVD risk.

Cholesterol is just one of many factors that effect the risk but we know that irrespective of cholesterol level, starting a statin will substantially lower the risk.

A patient  who has smoked   cigarettes lifelong  asked me this question recently.

When I plugged the patient’s excellent cholesterol values into the ASCVD app, the 10 year risk of heart attack or stroke was quite high, 14.9%. Bad cholesterol  (LDL) was 90, well below what is considered optimal. Good cholesterol (HDL) was 60, well above what is considered optimal.

Studies have demonstrated that even patients with cholesterol numbers this good benefit from statin therapy. Their risk of heart attack and stroke will be substantially reduced over time.

My patient has not yet had a heart attack or stroke and it is likely that despite engaging in the extremely damaging behavior of cigarette smoking , the genetically programmed excellent cholesterol values have somewhat protected from ASCVD.

However, a vascular screening study has demonstrated  that  early atherosclerotic plaque in both the patients carotids. The patient has ASCVD and it is only a matter of time if the patient keeps smoking before the patient  has a clinical event related to it.

I told my patient that if he/she stopped smoking cigarettes his/her estimated 10 year risk would drop to 9.7% and I would not recommend statin therapy.

We discussed methods to help quit and the patient indicated that the patient would start  using a nicotine patch and try to quit in the next few months.

Unfortunately, at follow up smoking was ongoing.

Thus, my recommendation to start statin therapy despite her excellent cholesterol values.

Other groups of patients besides cigarette smokers can have advanced or premature ASCVD with excellent or “normal” cholesterol values. Diabetics often have low bad cholesterol values associated with low good cholesterol and high triglycerides.

Sometimes, ASCVD develops prematurely even in patients who have a low 10 year risk based on standard risk factors. This is usually in patients with a strong family history of ASCVD who have an inherited atherogenic abnormality of lipid metabolism that is not manifested in the standard cholesterol parameters (see Dealing With the Cardiovascular Cards You’ve Been Dealt).

To identify these patients a search for subclinical atherosclerosis by vascular screening or coronary calcium scan is necessary. When advanced plaque is identified statin therapy is often warranted even with a low estimated 10 year risk and normal cholesterol values.

So some patients can have very high cholesterol values and I don’t recommend any therapy, some have low and I do. I’m much more focused on the presence or absence of ASCVD in my treatment decisions.

Ultimately we are not treating “high cholesterol” when we start cholesterol lowering therapy we are working to prevent or slow the progression of ASCVD,

-atherosclerosis is still my psychosis





Are You Sabotaging Your Heart With Statin Drugs?

No, you are not “sabotaging” your heart with statin drugs. Neither are you “wrecking” your heart.

But that title probably got your attention if you are taking a statin drug and thought that it was helping your heart.

Typical appearance of Newsmax Health. Note that  the offer to assess cardiac risk is a self-serving promo of the book on natural cardiac cures written by the author of the article on the left which summarizes only the negatives of bypass surgery
Typical appearance of Newsmax Health. Note that the offer to assess cardiac risk is a self-serving promo of the book on natural cardiac cures, written by the author of the article on the left, which summarizes only the negatives of bypass surgery

This question is prominently displayed on the Health portion of a news website called Newsmax, that somehow interrupted my web surfing today. If you click on the banner, you will get to listen to the words of Dr. David Brownstein, “America’s most popular family physician.”

Dr. Brownstein, in my opinion, should more properly be termed “one of America’s most popular quacks, charlatans and purveyors of misinformation in order to market useless junk.”

What Brownstein says can be found on multiple similar sites across the internet which are promoting “alternative” or “natural” approaches to high cholesterol.

His claims can be summarized as follows:

  • statin drugs do nothing to protect you from heart attacks
  • statin drugs “weaken your heart,” muscles, cause fatigue and lower your sex drive, damage your kidneys and liver
  • statin drugs prevent the formation of cholesterol which is essential for brain, sex hormone and vitamin D production
  • 1/2 of people with heart attacks have normal cholesterol levels
  • CHF is increasing in frequency and it is related to an increase in statins and consumption of sugar and refined carbohydrates
  • Big pharma has perpetrated the biggest fraud in medical history on the American public by brainwashing doctors, beginning in medical school, to prescribe statin drugs

These claims resonate with patients who are reluctant to take medications and who feel that “natural” approaches to prevention and treatment are superior.

Brownstein uses a combination of alarmist rhetoric and pseudoscientific jargon that appeals to those seeking alternatives.

Let’s look at his claims.

Do Statins Prevent heart Attacks?

Statins unequivocally prevent heart attacks in patients who have had heart attacks or have evidence of advanced vascular disease due to atherosclerosis. This is called secondary prevention and there are almost no cardiologists/scientists with any credibility who dispute the value of statins in secondary prevention.

The only specific study that Brownstein cites is the ASCOT-LLA study, published in 2003 which looked at ten thousand patients with hypertension, no heart disease and low or normal cholesterol levels, half of whom got 10 mg of atorvastatin and half a placebo.

This was a primary prevention study and showed such a benefit of the atorvastatin on reducing heart attack and coronary deaths that the study was stopped early, at 3.3 years at which time 154 patients receiving placebo versus 100 receiving atorvastatin had had heart attacks or died from coronary disease.

This was a highly significant reduction in events. There are several ways to look at this data and present it to patients; Brownstein implies that “Big pharma” presented the most favorable way, which is that there was a 36% reduction in relative risk.

The absolute risk of an event in the atorvastatin group was 1.7% (2.7% in the placebo group), so the absolute risk reduction was from 2.7% down to 1.7% or 1%.

To help better understand the data, we can also look at the number needed to treat (NNT). The NNT is the inverse of the absolute risk reduction. So for the ASCOT trial, the absolute risk reduction was 1%. 1 divided by 1% is 100 — 100 people would need to be treated with atorvastatin (the generic of Lipitor) over the study period to prevent one heart attack. (For more discussion on the NNT check out this blog post and this paper on its limitations)

lipitorUnderstandably, Pfizer, the makers of atorvastatin, prominently displayed the 36% relative risk reduction in their direct to consumer marketing campaigns (featuring Dr.Robert Jarvik (proclaiming himself a doctor in direct to consumer videos), although he was never a licensed physician (see here for interesting discussion on the controversy that ensued)).

Until, the FDA compels them to do otherwise, big pharma will project their products in the most favorable light possible.

However, it is debatable whether presenting data to patients using absolute risk reductions or NNT info plus relative risk reductions results in better choices. As Mcalister has pointed out:

“For example, many British patients with atrial fibrillation who were likely to benefit from anticoagulant therapy because of their risk profiles and their similarity to the participants in randomized trials supporting the efficacy of warfarin declined warfarin therapy when presented with the data about their absolute risks and benefits.”

ASCOT really makes a strong case for taking a statin drug to prevent heart attacks, even in those with normal or low cholesterol levels, not the opposite, as Brownstein has implied.

Do Statin Drugs “Weaken” The Heart Muscle Or Cause Heart Failure?

After criticizing the now infamous “Seven Nations Study” of Ancel Keys, which found high fat consumption in countries with high rates of heart attacks, Brownstein trots out the weakest imaginable argument for statins causing heart failure: heart failure has increased in the last decades, statin use has increased, therefore statins are causing heart failure. 

Correlation does not equal causation!

There is no compelling evidence that statins cause heart failure or weaken heart muscle.

In fact, a recent review of heart failure and statins concluded that statins, while not reducing mortality in heart failure, do have favorable effects on reducing the rate of hospitalization for heart failure and increasing the strength of the heart muscle.

Statins may not be as beneficial in patients with heart failure, but they definitely don’t cause heart failure.

Much of the misinformation about heart failure and statins arises from sites like Life Extension, which promotes sales of its own preferred brand of vitamin CoQ10, ubiquinol. (According to their website, though, this is for altruistic reasons: “We at the Life Extension Foundation take a different view. Keeping our members in a youthful state of longevity is the most efficient way of maintaining the revenue stream we need to fund our scientific research projects. We had no problem reducing our margins to provide members with the clearly superior ubiquinol form of CoQ10.”)

As is typical for this slick organization (see my previous post here), the writing has the veneer of science but is all pseudoscience with references that are outdated, irrelevant or meaningless.

Statin Side Effects

I’ve written about statin side effects and the decision to take them based on analysis of risks and benefits here and here.
By far, the most common thing we see is myalgia, aching of the muscles, and this is reversible.
The bottom line is that the benefits of statins far outweigh the risks if you are at very high risk for heart attack and stroke.  The risks outweigh the benefits if you are at very low risk.
For those in the middle, I advocate a search for subclinical atherosclerosis either by vascular screening or coronary calcium detection.

Misinformation and Scare Tactics on the Internet

Brownstone is not the only purveyor of dangerous misinformation on Newsmax’s Health website. There seems to be a concerted effort to promote quacks and charlatans and any information on this website is suspect.

A good rule of thumb if you are searching for credible health information on the web:

Avoid sites that use scare tactics and inflammatory rhetoric to induce you to stop your prescription medication and buy a health newsletter or nutraceutical.

By the way, Big Pharma has not brainwashed me.

I have no ties to industry.

I stopped taking any pharma food or money years ago.

Listen all y’all, it’s not a sabotage!

-Boyishly yours,



Since Dietary Cholesterol Isn’t Important Can I Stop Taking My Cholesterol Drug

A year ago one of my patients began experiencing  chest pain when he walked up hills. Subsequent evaluation revealed that atherosclerotic plaque (95% narrowing of a major coronary artery ) was severely reducing the blood flow to his heart muscle and was the cause of his chest pain. When this blockage was opened up with a stent he no longer had the pain.

Along with other medications (aspirin and plavix to keep his stent open) I had him start atorvastatin, the generic version of Lipitor, a powerful statin drug that has been shown to prevent progression of atherosclerotic plaque and thereby reduce subsequent heart attacks, strokes and death in patients like him

I saw him in the office the other day in follow up and he was feeling great . He asked me “Doc I read  your post yesterday.s Since you say that cholesterol in the diet doesn’t matter anymore, does that mean I don’t have to take my cholesterol drug anymore.?”

His question gets at the heart of the  “diet-heart hypothesis”. The concept that dietary modification, with reduction of cholesterol and fat consumption can reduce coronary heart disease.

The science supporting this hypothesis has never been strong but the concept was foisted on the American public and was widely believed. It was accepted I would  say because it has a beautiful simplicity which can be summarized as follows:

“If you eat cholesterol and fat it  will enter  your blood stream and raise cholesterol levels. This excess cholesterol will then  deposit in your arteries, creating fatty plaque , clogging them and leading to a heart attack.”

This concept was really easy to grasp and simplified the public health recommendations.

However, cholesterol blood levels are determined more by cholesterol synthesized in the liver and predicting  how dietary modifications will effect these levels is not easy.

Since the public has had the diet-heart hypothesis fed to them for decades and given its beautiful simplicity it is hard to reverse this dogma. My patient’s question reflects a natural concern that if science/doctors got this crucial question so wrong, is everything we know about cholesterol treatment and heart disease wrong?

In other words, are doctors promoting a great cholesterol hoax?

Evidence Strongly Supports Statins in Secondary Prevention 

For my patient the science supporting taking a  cholesterol-lowering statin drug is very solid. There are multiple excellent studies showing that in patients with established coronary artery disease taking a statin drug substantially reduces their risk of heart attack and dying.

These studies are the kind that provide the most robust proof: randomized, prospective and blinded.

level of evidenceWhen cardiologists rate the strength of evidence for a certain treatment (as done for lifestyle intervention here) we use  a system that categorizes the evidence as Level A, B, or C quality.

LeveleA quality (or strong) evidence consists of multiple,large, well-done, randomized trials such as exist for statins in patients with coronary heart disease.

Level B Evidence comes from a single randomized trial or nonrandomized studies.

Level C evidence is the weakest and comes from “consensus opinion of experts, case studies or standard of care.”

When treatment recommendations are based on Level C evidence they are often reversed as more solid data is obtained. Level A recommendations almost always hold up over time.

The level of evidence supporting restricting dietary cholesterol and fat to reduce heart attacks and strokes has always been at or below Level C and now it is clear that it is insufficient and should be taken out of guideline recommendations.

Evidence Strongly Supports Atherogenic Cholesterol is Related to Coronary Heart Disease

There are other lines of evidence that strongly support  the concept that  LDL cholesterol (bad cholesterol) or an atherogenic form of LDL cholesterol is strongly related to the development of atherosclerosis. If you are born with really high levels you are at very high risk for coronary heart disease, conversely if you are born with mutations that cause extremely low levels you are highly unlikely to get coronary heart disease.

Thus, the cholesterol hypothesis as it relates to heart disease is very much till intact although the diet-heart hypothesis is not.

Conflating the Diet-Heart Hypothesis and the Cholesterol Hypothesis

There is an abundance of misinformation on the internet that tries to conflate these two concepts. Sites with titles like “The Great Cholesterol Lie” , “The”  Cholesterol Hoax”, The Cholesterol Scam”  abound .

These sites proclaim that cholesterol is a vital component of cell membranes (it is) and that any attempt by diet or drugs to lower levels will result in severe side effects with no benefit

Doctors, according to these types of sites, in collusion with Big Pharma, have inflated the benefits of statin drugs and overlooked the side effects in the name of profit. Often, a “natural” alternative to statins is promoted.  In all cases a book is promoted.

The Great Cholesterol Truths

It’s unfortunate that nutritional guidelines have promoted restriction of cholesterol and fat for so long. These guidelines (like most of nutritional science)  were based on flawed observational studies. They should not have been made public policy without more consensus from the scientific community.  The good news is that ultimately the truth prevails when enough good scientific studies are done.

It is right to question the flimsy foundation of nutritional recommendations on diet and heart disease but the evidence for statin benefits in patients with established coronary heart disease is rock solid.

Hopefully, the less long-winded explanation I provided my patient in the office will persuade him to keep on taking his atorvastatin pills while simultaneously allowing him to eat eggs, shrimp and full fat dairy without guilt.

Should All Men Over Sixty Take a Statin Drug?

The updated AHA/ACC Cardiovascular Prevention Guidelines (CPG) which include the   excessively wordy “The Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults Risk” were published late last year and immediately were the center of controversy.

After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.

As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.

Should we be starting all elderly Americans on statin drugs?

My simple answer is no. It doesn’t make sense to do this, because clearly not all elderly individuals have atherosclerosis or will ever develop its consequences of heart attack and stroke. Many have inherited the genes that allowed their parents to live free of heart disease into their 90s and will not benefit at all from long term statin therapy; they may actually suffer the expense and side effects instead.

How can we better decide who among the elderly will benefit from statin therapy?

If you have read my previous posts on searching for subclinical atherosclerosis here and here you probably know the answer. Let’s look at a specific case and apply those principles.

Robert is 69 years old. I see him because, in 2010, the posterior leaflet of his mitral valve ruptured, resulting in the mitral valve becoming severely incompetent at its job of preventing back flow from the left ventricle into the left atrium. I sent him to a cardiac surgeon who repaired the ruptured leaflet. Although he has a form of “heart disease,” this is a form that has nothing to do with cholesterol, hypertension or diabetes and is not associated with ASCVD.

However, it is my job to assess in him, like all individuals, the risk of developing coronary heart disease or ASCVD.

He has no family history of ASCVD and he feels great since the surgery, exercising aerobically 4-5 times per week.

His BMI is 23.87 which is in the normal range. His BP runs 116/80.

His total cholesterol is 210 and LDL or bad cholesterol is 142. Good or HDL cholesterol is 56 and triglycerides 59. The total and LDL cholesterol levels are considered “high,” but they could be perfectly acceptable for this man.

When I ran his 10 year ASCVD risk (risk of developing a heart attack or stroke over the next 10 years), it came back as 14%. The new guidelines would suggest having a conversation with him about starting a statin if his risk is over 7.5%. His risk is double this and statins are definitely recommended in this intermediate risk range. Interestingly, I cannot enter a cholesterol level or blood pressure for a man of this age that yields a risk less than 7.5%.

When I had my discussion with him about his risk for ASCVD, I plugged his numbers into my iPhone and showed him the results and gave him the guideline recommendation.

Lifestyle Changes to Lower Cholesterol

The new Cardiovascular Prevention Guidelines have a section devoted to Lifestyle Management to Reduce Cardiovascular Risk. Unfortunately, none of the lifestyle changes they recommend have been shown to reduce ASCVD risk in an individual like Robert. He already exercises the recommended amount, is at his ideal body weight and eats a healthy diet. If we were to tighten up on his diet by, say reducing red meat, eggs and high fat dairy, all we would accomplish would be to lower his LDL and HDL cholesterol levels and make his life and meals less satisfying. The lower total cholesterol and LDL cholesterol would not lower his risk of ASCVD and the calculated 10 year ASCVD risk would still be in the range where statins are recommended.

Therefore, I am not going to tell Robert that he should reduce his saturated fat consumption (he already has incorporated that into his diet since he’s been bombarded with the low fat mantra for 30 years).

Searching for Subclinical Atherosclerosis

I’m going to tell Robert that we need to know if he has atherosclerosis, the disease that we are attempting to modify.

We started with an ultrasound to look at the lining of the large arteries in his neck that supply blood to the brain, the carotid arteries (a process I describe in more detail here). Although severe atherosclerotic blockages in these arteries put one at risk of a stroke, I was much more interested in the subtle changes in the arteries that precede symptoms and are an early harbinger of atherosclerosis.

Careful ultrasound recording and measurement of the main common carotid arteries from both the left and right side showed that the IMT or thickness was lower than average for his age, gender and ethnicity. His carotid IMT was at the average for a 60 year old, therefore, his so-called vascular age was 60 years, younger than his chronological age. If I plug that age into the ASCVD risk estimator, I get an 8.2% 10 year risk, just barely above the statin treatment cut-off.

Careful scrutiny with ultrasound of the entire visible carotid system in the neck on both sides did not reveal any early fatty plaques or calcium in the lining of the carotid arteries. He had no evidence for atherosclerosis, even very subtle early forms, in this large artery, a finding which is usually predictive of what is going on in the other large arteries in the body, including the coronary arteries, which supply blood to the heart.

At this point, I think, we could have stopped the search for subclinical atherosclerosis and agreed that no statin therapy was warranted. However, Robert wanted further reassurance that his coronary arteries were OK, therefore we set him up with a coronary calcium study (see my full description of this test here).

Searching for Subclinical Atherosclerosis: The Calcium Score

Robert’s coronary calcium score came back at 21 (all in the LAD coronary artery) , which put him at the 26th percentile compared to normal men of his age and gender. A score of 21 is average for a 59 year old man and 82% of men aged 69 have a score greater than zero. Robert had much less calcium in his coronaries than men his age, another factor putting him in a low risk category.

Given the low risk findings from both the vascular screening and the coronary calcium, I felt comfortable recommending no statin therapy and going against the guidelines.

Statins: Better Targets for The Two-edged Sword

This is not an unusual scenario; many of my older patients without heart attacks, strokes or diabetes fall into the risk category that would warrant statin therapy and if they have no clinical or subclinical evidence of atherosclerosis, I don’t advise statin therapy. My patients are free to follow the guidelines and take statin drugs after this advice, but most are very grateful that another pill (which they likely have heard bad things about on the internet or from friends with adverse experiences) can be avoided.

Statins are wonderful drugs when utilized in the right population, but they also carry a  9% increased risk of diabetes and about a 10% real world risk of developing muscle aches and weakness (myalgia).

I think it is essential to aim these two-edged swords at the right targets if we are to maximize the overall health benefits.

Statin Drugs Have Benefits Beyond Cholesterol Lowering

For most of the last 25 years I have told patients when I recommend  a statin drug to them that they should take it in order to lower their bad cholesterol (and raise the good cholesterol) thereby lowering their risk of future heart attacks.

I based this statement on my understanding of large statin trials which demonstrated reduction in heart attacks seemingly closely tied to drops in the bad cholesterol level.

Although I was aware of the so-called “pleiotropic” (meaning effecting multiple pathways leading to atherosclerosis) of statins it was easier to point to the cholesterol lowering effects and unify that message with the recommendation to reduce fat and cholesterol in the diet , thereby lowering cholesterol in the blood and arteries and cut heart attack risks.

Thus emerged a very simple (and likely false) paradigm: Fat in the diet causes fat in the blood which causes fat in the arteries which causes fatty plaques in the coronary arteries which causes heart attacks when they get too big and block off the blood flow.

I, like most cardiologists and lay people  mistakenly assumed that since lower bad cholesterol levels associated with taking a statin drug were associated with lower heart attack risks then dietary changes aimed at lowering bad cholesterol levels would also lower heart attack risk.

It turns out that we don’t really know how the statins reduce heart attacks . As a recent review points out:

 some of the cholesterol-independent or “pleiotropic” effects of statins involve improving endothelial function, enhancing the stability of atherosclerotic plaques, decreasing oxidative stress and inflammation, and inhibiting the thrombogenic response. Furthermore, statins have beneficial extrahepatic effects on the immune system, CNS, and bone. Many of these pleiotropic effects are mediated by inhibition of isoprenoids, which serve as lipid attachments for intracellular signaling molecules. In particular, inhibition of small GTP-binding proteins, Rho, Ras, and Rac, whose proper membrane localization and function are dependent on isoprenylation, may play an important role in mediating the pleiotropic effects of statins.

Supporting the non cholesterol lowering effects of statins on reducing CVD are the following observations

-Most heart attack victims don’t have elevated bad cholesterol levels and dietary reduction of bad cholesterol doesn’t seem very effective at preventing heart attacks.

-Drugs, like Zetia or ezetimibe which lower cholesterol level by other mechanisms don’t seem to prevent atherosclerosis even though they substantially lower bad cholesterol levels.

-Statin drugs reduce heart attacks in patients who have normal or low bad cholesterol levels

What Causes Atherosclerosis?

An article (Innate and adaptive inflammation as a Therapeutic Target in Vascular Disease) published in JACC recently by Tousoulis,et al. summarizes the current understanding of how atherosclerosis develops and the multiple ways that statins may affect that process. They write

Atherosclerosis, once thought to be a lipid storage disease, is now considered a chronic low-grade inflammatory condition that affects the vascular wall. It is characterized by the deposition of cholesterol and lipids followed by infiltration of T cells and macrophages, all as a result of an endothelial injury response.

I’m including this figure from the article to give you some idea of how incredibly complicated the process is.

Overview of Mechanisms Involved in Atherosclerosis Low-density lipoprotein (LDL) is oxidized in the presence of reactive oxygen species (ROS) and binds to proteoglycans (heparin sulfate) while simultaneously stimulating the endothelium, leading to adhesion molecule overexpression and increasing its permeability. Apart from this action, oxidized low-density lipoprotein (ox-LDL) inhibits nitric oxide (NO) production, prohibiting vasodilation. Furthermore, cytokines and other chemoattractant molecules, such as MCP-1, are secreted, favoring leukocyte adhesion. Leukocytes come into random contact with the activated endothelium and, due to interactions with adhesion molecules, roll and tether and are subsequently firmly arrested. In addition, leukocytes transmigrate into the subendothelial space, where they differentiate into macrophages, which in turn take up ox-LDL, forming foam cells. Ox-LDL antigens are presented by macrophage major histocompatibility complex class II (MHC-II) proteins and are recognized by CD4+ T cells. These preferentially differentiate into Th-1 cells, pro-inflammatory cytokine production. Finally, smooth muscle cell (SMC) proliferation and migration are induced as a result of cytokine and growth factor secretion.

Can you imagine trying to explain this to the average patient?

My eyes glazed over once I reached MCP-1.

Thus, doctors end up giving the simple, accepted conventional wisdom that we are “treating” high cholesterol by giving statin drugs. What we are really treating is atherosclerosis. And statins are the only effective drug treatment we have identified for this ubiqitous  and complex process.

It is entirely possible that the lower LDL cholesterol caused by statin drugs is totally unrelated to their ability to forestall atherosclerosis. The new cholesterol guidelines reflect this concept as they don’t recommend treating to an LDL target level.

I end with the closing comments from the article by Tousoulis, et al.

Given the fact that atherosclerosis is a multivariable disease, with several molecules involved in each stage, it is vey difficult to find an effective treatment. However, statins prove to be the most effective treatment so far because they interfere with most of the critical components of the atherosclerotic process and have been proven to have beneficial effects. Further to their well-established impact on nonspecific low-grade inflammation, statins also appear to have significant effects on innate and adaptive immunity that have been underestimated so far.