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,
-ACP
west of scotland
http://care.diabetesjournals.org/content/32/10/1941.full
On the Power of Cauls, Dickens’s Doctors, and Placebos
In the first chapter (I AM BORN) of Charles Dickens’s David Copperfield, the protagonist notes that “I was born with a caul, which was advertised
9 thoughts on “Does Pravastatin Lower Your Risk of Diabetes?: The Joys of Continuing Education From Patients”
With all the banter about “co-morbidities” in the COVID news, receiving a prediabetes diagnosis after 25+ years of hyperlipidemia treatment with simvastatin, and just lately rosuvastin, has brought confusion and fear. Primary care doctor claims getting LDL below 70 with rosuvastatin is worth the increased risk of progression to diabetes. Wife and I drastically altered diet to keep BG under 140 to reduce progression to diabetes risk, so the thought that rosuvastatin might invalidate the self-imposed culinary pleasure deprivation is confusing. Your assessment of “the benefits outweigh the risks” is calming, but it is hard not to think I’m trying to choose what I wish to die from.
I knew about the increased risk of diabetes with statins when my cardiologist wanted me on one due to somewhat elevated LDL. I told him I would if he would personally underwrite my diabetes treatment. No.
Though already thin, I can only keep my numbers at the cusp of “pre-diabetes” with additional diet restrictions.
Later, when he showed me my high CAC score, I said OK, if it’s pravastatin.
No.
He doesn’t prescribe the stuff because it’s so “minimally effective”.
So I took atorvastatin and felt sick, weak, and sore for six months.
I found that and the NNT and the NNH for statins in general to be the real deal breakers.
Besides, isn’t the risk of heart disease drastically increased in diabetes?
And, doesn’t statin treatment increase calcification? Do I want more?
No.
I view my CAC as an artifact of my past history — when I was following antiquated but only recently somewhat reversed medical guidelines for diet. (I’m gratified that you’re helping that particular reversal.)
1970’s research showed that a diet based on vegetable oil reduced cholesterol levels markedly more than a saturated fat diet. Recent revelations about that research show that those on the cholesterol reducing diet actually died sooner than those on the cholesterol increasing diet. What can be concluded about cholesterol lowering from that?
What actual endpoint should one consider when one prescribes?
What actual value do surrogates like cholesterol levels have?
What’s being taken for granted simply because it’s been… taken for granted?
Lots of interesting points there. I’ll address a few
1. I’m sorry your cardiologist won’t prescribe pravastatin. “minimally effective” but tolerated is better than powerfully effective but not tolerated.
2. The coronary calcium certainly is a reflection of atherosclerotic risk over decades, not necessarily what is going on right now, analogous to HB A1C and diabetes. However, more important than coronary calcium is the burden of soft or vulnerable plaque in the coronaries. Recent studies suggest that statins accelerate calcium deposition because they are “healing” the inflamed unstable lipid laden plaques and converting them to a more stable plaque characterized by calcium deposition.
3. I’ve emphasized in my writing that with drug or diet our goal is reducing atherosclerosis-heart attacks and strokes, not reducing cholesterol levels.
It’s a hard concept to communicate because the reduction of the surrogate end point (total or LDL cholesterol) feels reassuring and gives patients a goal to aim for.
Thanks.
Further: 🙂
(2.) I get it that calcification is an element of the healing process. Is that indeed what is happening with statins? Do we know? After all, it had been carved in stone that cholesterol lowering did the job.
(3.) From the article’s discussion:
“Though the MCE intervention effectively lowered serum
cholesterol in all prespecified subgroups, there was no
clinical benefit in any group.
Paradoxically,
MCE participants who had greater reduction in serum cholesterol had
a higher rather than a lower risk of death.”
http://www.bmj.com/content/bmj/353/bmj.i1246.full.pdf
Seems to me that it’s a paradox only if one’s expectation is in the wrong place to start with.
I was a “hyper-responder” to atorvastatin – LDL in double digits; HDL over 100. But If such LDL lowering is not statins’ benefit, what is?
The anti-inflammatory effect has been touted as the (modest) benefit. But inflammation is an essential part of the healing process. “Something” upstream causes that inflammation, no? Unless atherosclerosis is exclusively an auto-immune phenomenon?
I wrote a post a while back entitled “Statin Drugs Have Benefits Beyond Cholesterol Lowering” that addresses these questions. (https://theskepticalcardiologist.com/2014/08/02/statin-drugs-have-benefits-beyond-cholesterol-lowering/).
I was utilizing the most recent review paper on atherosclerosis. I don’t pretend to be an expert on this incredible process but what I got from reviewing this review was a sense of how incredibly complex atherosclerosis is, how much we have learned about it but how little we truly understand.
“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.”
Also, I wrote:
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.”
LDL lowering by statins may just be a marker for the overall effectiveness of the drug in all these processes or it may be just be part of the overall benefit.
Did Donna abandon changing her diet (and exercise) regime before going to the statin?
She did. We rechecked her lipid profile and she was still in a high risk category.
But what I see in her and others like her who are really already eating a good diet and not overweight and physically active is that it is not her lifestyle and diet that is the problem, it’s the cardiovascular cards she was dealt. .
If you are at ideal body weight, moderately physically active, not smoking cigarettes, controlling stress in your life and without diabetes there is not much diet or lifestyle change will do to modify your risk.
I know this goes against the wellness mantra.
Great blog! Next time please discuss the cardiovascular benefits of the Viking River Cruise. Thanks!
Will do! Now if only I could get funding for that research from the NIH.