Like most family physicians, I spend an absurd amount of time each day discussing statins with patients, usually around the issue of side effects they have heard about from TV, magazines or the Internet. However, rather than roll my eyes at yet another statin question, I look at it as a terrific opportunity to provide my patients with a quick summary of the evidence. (Credit to Dr. James McCormack and Dr. Michael Allan from the Best Science Medicine podcast for completely changing my approach to prescribing and evaluating cardiovascular risk).
One could argue that statins have become a microcosm of the polarity of health care decision-making as a whole, with two sides diametrically opposed with little common ground. One group sees statins through the lens of “statins being terrible for you”, and the other through statin-coloured glasses.
Let me try to bridge this divide.
Statins are effective for secondary cardiovascular prevention, and anyone who debates this is being intellectually dishonest.
The effectiveness of statins for primary prevention is dependent on someone’s baseline cardiovascular risk. We can’t say that statins are good, or that statins are bad. Whether to use statins depends on the patient’s risk. The (approximately) 20% relative risk reduction from statins is certainly more impressive in a patient with a 30% 10-year risk compared to someone with a 5% 10-year risk.
“Doc, do I need to take a cholesterol pill?”
Don’t look at statins as a “cholesterol pill”, but as a pill to potentially reduce your cardiovascular risk. Someone can have a pretty good lipid profile, but still be high-enough risk to warrant consideration of a statin. Or conversely, they can have a borderline high lipid profile, yet have such a low cardiovascular risk that statins would be of little use.
I will briefly tell my patients whether the “guidelines would say” they need to take a statin or not. Then I will use this calculator from the Best Science Medicine team (http://chd.bestsciencemedicine.com/calc2.html) to show them what their baseline risk is, and what benefit they would receive from a statin.
Then….and you’ll never believe this…I let the patient decide. Patient-centred medicine! It is possible! Many patients will put it back to me and ask “What would you do?”, which makes it a bit trickier, but patients generally love having a visual representation of what this proposed pill is doing. If I think they are sufficiently high risk, I may encourage the statin more forcefully, but it is generally a very patient-centred discussion in my office. The idea of doing something “because the doctor said so” is quickly falling out of fashion.
Why is this so important? Because if the patient doesn’t know why they’re taking the statin, they are much more likely to be swayed by the next thing they hear about statins in the media, or from their friends. If they can’t personally explain why they take a statin, there’s very little chance that they will continue to be compliant in the face of controversy.
Which brings us to this issue of statins and diabetes. The evidence is strongly pointing to the fact that statins likely raise blood glucose levels, by around 0.1-0.3 mmol/L. The headlines have screamed “Statins cause diabetes”, including a lawsuit launched last week by London, Ontario law firm McKenzie Lake against Pfizer, maker of Lipitor.
But what does this really mean? We make a diagnosis of diabetes based on glucose readings, and someone whose fasting blood glucose goes from 6.9 to 7.0 is now magically diabetic. Hence the increased incidence of diabetes with statins. And with the marketing surrounding diabetes, patients are terrified by this. But did their microvascular or macrovascular risk appreciably change there? The overwhelming majority of diabetic complications are macrovascular in nature, and since we know that statins decrease macrovascular events, doesn’t it follow that we shouldn’t be overly concerned about a tiny increase in blood glucose? We have good evidence that patients who are prescribed statins typically exercise less and eat lesser-quality foods than they did pre-statin (the “Lipitor will take care of things” assumption), so this certainly could account for some of the worsening in glycemic control. Also, patients who are deemed to be of a high cardiovascular risk are often the same patients at risk of developing diabetes, so it’s very tough to tease out a causal effect of the statins with observational or retrospective data. Do statins increase blood glucose? Probably, yes. But we need to keep the magnitude of this in perspective.
Here’s my bottom line to my patients. If we’ve made the decision to start a statin, it was made by taking into account their cardiovascular risk, and together we felt that the risk was high enough to justify taking a daily statin. If there is any compelling reason to discontinue statins as a class, I can search my electronic medical record for all of my patients on statins, and I will call each of them personally. The potential for an increase in blood sugar because of statins, however, shouldn’t change our decision to prescribe a statin for its potential cardiovascular benefit.
Oh, and whether you’re on a statin or not, you should be exercising at least 4 days a week (30-45 minutes per session) and eating a healthy diet. The statin doesn’t replace a good lifestyle. They both reduce cardiovascular risk, and actually augment each other. Check out the calculator for some neat risk reduction math with lifestyle measures.