The debate about statins continues. Mark Hyman published a piece that says that statins raise the risk for diabetes (we knew this) but statins mostly do not prevent cardio disease and events in people who have somewhat high cholesterol but not heart disease. Inflammation is the main culprit, not cholesterol. He never mentions PCSK9i drugs such as Repatha. Since these also can raise blood glucose and the risk for diabetes can we assume what he says about statins also apply to PCSK9 inhibitors? And what do we think of his position on statins?
As a 76 yr old female who had mildly elevated cholesterol (but with Lp(a) of 40) I have been taking Repatha, Exetimibe, and to counter the elevated (prediabetes level) glucose, which went higher on the cholesterol meds, I have been taking Metformin and also, sometimes Berberine.
Wondering if I should stop taking and just do everything possible to reduce inflammation (many of which am already doing).
If inflammation was the key, why do the LMHR still develop plaque at nearly the same rate as diabetics?
There are also multiple interventions like PCSK9i that don’t necessarily change inflammation levels but still cause plaque regression. And some statins don’t even raise the risk of diabetes (pitavastatin and pravastatin).
Have you tested your hscrp to see if you have chronic inflammation? Seems like this is where you should start if you’re worried about inflammation.
Hyman is probably basing this on the new guidelines from ACC. You can read a summary of it here to familiarize yourself
hs-CRP is actually a stronger predictor of cardiovascular events than LDL
Why? In some ways, cholesterol has become a victim of its own success. We now screen the whole population for high cholesterol, give statins to those with high LDL (or ApoB), and so then the majority of people who end up having heart attacks have lower cholesterol than they would naturally have. This means most of the majority of residual risk for heart attacks will be found in biomarkers that aren’t SMuRFs.
Inflammation (hs-CRP) is one such non-SMuRF, perhaps one of the strongest. This is especially true for people already on statins or those without traditional risk factors (sometimes called “SMuRF-less” patients). In these groups, cholesterol may be well controlled, but inflammation remains a key driver of events.
Note that this applies to people already taking a statin, and statin use is still necessary. Looking at Hscrp only enters the picture after initiation of statin use, you are not better off getting off lipid lowering medication.
Guess what statins do? They lower CRP in addition to LDL/ApoB. They do work for primary prevention, but the fewer the risk factors in the group studied, the longer the time period required and the larger the sample size required to demonstrate statistical significance.
Inflammation (and things like high blood pressure) damages the vessel wall and exacerbates the process. Cholesterol (well, lipoproteins) are the building blocks of the plaque which eventually ruptures and kills people. Personally, I would argue that the building blocks are the most important factor. But there’s a recent scientific statement paper which does spell out a case that both are important (attached).
I think the evidence shows that a person can have high inflammation, but if they don’t have high lipoproteins then you won’t build plaque, because they lack the building blocks. (Of course, you can still have other cardiovascular diseases and negative consequences from the inflammation).
So, as the paper makes clear, in an ideal treatment/health scenario you should be managing both inflammation and lipoproteins. It doesn’t make sense to me to say that you shouldn’t worry about the lipoproteins. For example, if you look at children with familial hypercholesterolemia, they often have cardiovascular events in their teens, 20s or 30s - and they all have a baseline of very low inflammation. Cholesterol alone is enough to give you an early death, basically.
I don’t know enough about this guy to critique his credentials or expertise. But if we value the opinion of authority figures, I reckon we have the American Heart Association, European Society of Cardiology who assemble panels of expert basic researchers, clinicians, clinical researchers, pathologists, statisticians etc and every few years they come out with a massive document of guidelines. To my knowledge, every single one of them recommends statins. Plus most countries have their own guidelines, like the UK NHS (through something called NICE), who weigh up evidence and make recommendations. They also strongly promote the use of statins for primary prevention. In fact, in the most recent guidelines, every single set of guidelines is getting more aggressive with use of statins, and recommending lower and lower targets.
Now, there does exist some % of the population who go around with horrible lipids on paper but don’t really build much plaque. However, they are maybe 5%, and we don’t really understand why. Perhaps something to do with the actual function of their lipoproteins, or macrophages in the vessel walls. Those are things which we simply can’t measure using blood tests or any of the tools we have available, so I wouldn’t count on being one of those “lucky” people unless you have a really good rationale.