Login | April 30, 2026
Statin’s negative side effects possibly understood
PETE GLADDEN
Published: April 27, 2026
Statins have had a pretty good track record for helping individuals in lowering their cholesterol levels to offset the potential for a stroke/heart attack due to blood vessel blockages.
And they do that by blocking a specific liver enzyme that’s needed by the body to produce cholesterol.
This then reduces one’s LDL levels (“bad” cholesterol), which subsequently helps to slow down, prevent or even eliminate the build-up of fatty deposits inside of blood vessels.
And having taken this drug for a number of years, I’m speaking from experience when I say that I’m fortunate for its existence, primarily because I’ve had some pretty nasty coronary artery blockages - despite my lifelong participation in cardiorespiratory fitness activities.
Do I like taking stains?
I don’t.
Yet that's a moot point due to the fact that my situation is pretty serious.
Not taking statins risks me ending up back in the OR for more life-threatening coronary arterial blockages.
Now as far as my dislike for statins, that stems from the fact that I’m the one out of ten unlucky statin users who experiences intermittent muscle pain, fatigue, cramping along with muscle weakness and even muscle atrophy.
Sometimes the side-effects feel crippling, thus my like-dislike relationship with statins.
And I’ve been working with my cardiologist for years now to try to fine tune their usage.
Some of the tweaks involve my taking the drug every other day instead of every day, and ingesting a couple of daily supplements like CoQ10 and magnesium.
Those minor fixes have provided me with some relief but I still experience statin’s gnarly side effects, only now at less frequent and less severe magnitudes.
So I’ve always been hoping that medical science would come to understand why statins produce problems for individuals like me, and then subsequently remedy the drug’s painful side effects.
All of which brings me to a newly released study that just might be the first step in understanding exactly why statins can impart these negative side effects to some users.
The study, “Cryo-electron microscopy reveals sequential binding and activation of Ryanodine Receptors by statin triplets,” was published in the November 20, 2025 issue of
“Nature Communications.”
So past research has reveled that statins do not act on the liver exclusively, they also interact with certain of the body’s proteins, most notably a protein that plays a key role in muscle function - Ryanodine receptor 1 (RyR1).
Now this particular protein dwells within a muscle’s sarcoplasmic reticulum, an apparatus that stores, releases, and takes in calcium ions.
And under normal circumstances this RyR1 protein tightly controls calcium release and uptake, thereby allowing for the controlled relaxation and contraction of muscles.
But sometimes this controlled action can be disrupted, and researchers had been unable to determine if it was precisely the RyR1 binding to the statins that accounted for statin’s negative side effects.
So in the aforementioned study, researchers used mice to investigate how statins might cause a disruption of this RyR1 protein.
What they found was that certain statins did indeed bind to the RyR1 protein in such a way as to destabilize a sarcoplasmic reticulum’s calcium storage/release/uptake properties, thereby resulting in muscle cell damage via calcium leaks.
The result of this destabilization is the side effects that I experience - soreness, cramping, tenderness, and reduced muscle strength.
Not only that, but they also found that there exists degrees of vulnerability amongst individuals, especially in people with genetic mutations which affect this RyR1 protein.
Indeed, as some people with severe vulnerabilities can experience even worse maladies than I, like malignant hyperthermia (dangerous body temperature spikes) and/or impaired diaphragm function.
So where do we go from here?
According to the study’s researchers there are at present two potential solutions to this statin vulnerability issue.
The first potential solution involves redesigning statins such that they continue to block cholesterol production but don’t interfere with the RyR1 protein.
The second potential solution involves figuring out a way to protect the muscle cells directly.
Now with respect to this second potential solution, the researchers tested an experimental class of drugs called “Rycals” in mice that were unable to tolerate statins.
And these compounds did indeed help stabilize the calcium channel, preventing leaks and reducing muscle weakness.
As it stands now, this study has given me a bit of hope that the solution for us unlucky one-out-of-ten statin users isn’t too much further down the road!
Pete can be reached at pjgladd@aol.com.